Hyderabad, Oct 29 (PTI) One of Asia's premier
healthcare groups, Apollo Hospitals, today launched a 'stroke
robot' which will assist experts to diagnose and advise
treatment for brain stroke patients within the country and
outside, its chairman said.
"RP-7, a state-of-the-art, wireless and internet-based
robot allows neuro-physicians sitting in the comfort of their
offices to speak to the patient, nurse and the doctor on duty
with the help of a monitor located in the place of the head of
the contraption.
The physician after logging in into his computer or
laptop can virtually make the robot move to any corner of the
room with the help of the cursor," authorities said.
"It is important that a brain stroke patient reaches
the nearest neurology centre within four hours. These robots
will help us cut short the time as vital signs of the patient
can be checked and diagnostics could be advised within
minutes. Doctors can also speak with family members, check
bedside monitors and ventilator settings," said Dr Subhashini
Prabhakar, Head of Neurology, Apollo Hospitals.
"Non-communicable diseases like brain stroke will be
making a hole in the pockets of Indians to the tune of USD 270
billion within a decade and finding suitable technology will
cut down the costs of treatment," Chairman of Apollo
Hospitals, Pratap C Reddy said.
Initially, the RP-7 will be placed here and in due
course of time seven major centers of Apollo Hospitals will
have similar robots helping the brain stroke patients, he
added.
Demonstrating a treatment protocol from a hospital in
China, Dr Deepak Arjun Das of Apollo Chennai said, "the FDA
cleared RP-7 also allows direct control to medical devises
such as electronic stethoscopes, ultrasound, MRI and even
transmit medical data to the remote physician".
Informing that the rate of deaths due to brain stroke
currently stands at 250 per one lakh population in the
country, Executive Director of Apollo Hospitals Sangitha Reddy
said, "Apollo Hospitals will bring down the incidence of brain
stroke deaths in the country". PTI CORR
NSK
Sunday, October 30, 2011
Brain scans make dream reading possible?
In a scenario where recalling dreams looks far-fetched, can a man-made device measure dream content? Well, experts at Max Planck Institute have gauged the mechanism of the brain involved in the process of dreaming. This experiment was possible due to dreamers who have the ability to modify the content of their dream by having knowledge of their state. These persons are also known as lucid dreamers. The team found that brain reactions while in a dream sequence was apparently in sync with the one observed during an actual implemented motion in a condition of wakefulness.
The lucid dreamers were asked to become aware of their dream while exposed to a magnetic resonance scanner and report this state of their mind through eye movements in the trial. They were then asked to dream about clenching their right fist followed by the left one for about 10 seconds voluntarily.
This helped the investigators gauge the entry into REM sleep where dreams are intensively felt. They achieved this by using the participant’s electroencephalogram (EEG) to identify the onset of a lucid episode. The brain activity calculated starting from this point was parallel to the premeditated dream that involved tilting the fist.
A specific portion in the sensorimotor cortex of the brain that plays a role in execution of movements seemed to be spurred during the dream. This can be implicated in the brain activity that occurs when the hand is shifted while the person is awake. Even in case where the lucid dreamer has just imagined an action of moving the hand, the sensorimotor cortex behaved in a similar manner.
“With this combination of sleep EEGs, imaging methods and lucid dreamers, we can measure not only simple movements during sleep but also the activity patterns in the brain during visual dream perceptions,” quoted
Martin Dresler, a researcher at the Max Planck Institute for Psychiatry.
This coincidence of the brain activity determined during dreaming and in the voluntary action implies that dream content is measurable. Another study participant was subjected to another technology known as near-infrared spectroscopy where the analysts found increased activity in a part of the brain that contributes to the planning of movements.
Thus, the scientists conclude that our dreams are not just an inactive phase but certain regions of the brain related to the dream content function in the process.
Saturday, October 29, 2011
Brain Waves Used to Steer Helicopter on Computer Screen, Offers Hope to the Disabled
Neuroscientists have experimented with brain waves for years, making slow progress. Now Dr. Bin He of the University of Minnesota and his team report a promising experiment.
They outfitted volunteers with caps with EEG sensors, and asked them to steer a helicopter on a computer screen through a series of randomly generated rings that appeared on the screen ahead of it. There were no hand controls, no joysticks. They could only try to will the helicopter forward with their minds.
It worked surprisingly well, Dr. He and his colleagues reported in the current issue of the online journal PLoS One. Eighty-five percent of the time, the volunteers could steer the virtual helicopter accurately.
"People have never done anything like this using noninvasive techniques," said He in a telephone interview. There have been other experiments before, but the most successful required that electrodes be surgically implanted in the brain. In one famous but sad case, Massachusetts researchers were able to get a young quadriplegic man to steer his own wheelchair -- but he ended the experiment, partly because he hated having wires inside his skull.
"Our technique was noninvasive," said He. The BCI -- short for brain-computer interface -- "is approaching the reliability that used to be done only by invasive procedures, though I will not say that it is better yet."
The challenge in using EEG signals is that they are, in the jargon of scientists, "noisy." The brain generates minute amounts of electricity as one thinks, and sensors can detect it, but readouts can look like random vibrations, and it is hard to tease out, say, a signal that means you want to turn left or right.
Earlier this year a team at the Berlin Institute of Technology in Germany reported they could detect drivers' intent to hit the brakes when they were at the control of a car simulator. But that was a relatively simple signal -- to brake or not -- and it came all of 130 milliseconds before the drivers actually tried to stop the car.
"While this may not seem [like] much, it may be enough to prevent accidents," said Stefan Haufe, the lead researcher, in an email to ABC News.
The Minnesota experiment was small -- three young female volunteers -- but the task was more ambitious. They set the EEG sensors to detect a particular brain wave called the sensorimotor rhythm.
"This was three-dimensional," he said . "The helicopter had to approach the ring, move forward, and go through without hitting it."
So it's one step at a time. But could it someday help a disabled person, without surgery, to use a robotic arm, or maneuver in the real world?
"We are always thinking of practical uses," said He. "That's the purpose of doing science."
Do not let stroke strike you down
Today is World Stroke Day
On the eve of World Stroke Day on October 29, doctors caution the public
on the factors that cause stroke and how to watch for the warning signs
and prevent disaster.
Neurologist at K.G. Hospital T.C.R. Ramakrishnan explains that stroke or
cerebrovascular accident or brain attack occurs when the vessels
supplying blood to the brain are blocked, interrupting the blood flow.
This results in the death of the brain cells. And, functions such as
speech, memory or movement may be affected depending on the area of the
brain involved.
Stroke is the second leading cause of death after the age of 60. Studies
across the world show that cases of stroke occur every six seconds. It
is not that stroke affects only elders. Stroke is the fifth leading
cause of death in people aged 15 to 59 years. Stroke is indiscriminate
and does not respect age, sex, race or economic status.
Stroke afflicts 15 million people each year. Of them, almost six million
die and a further five million are left permanently disabled.
In 2009, the World Stroke Organisation fixed October 29 for the start of a global campaign titled “Stroke, what can I do?” The following year, it launched the “1 in 6” campaign to emphasise that one in six people will have a stroke within their life time.
This year, the organisation is continuing with the theme of 2010 “One in
six”, but has added “Act Now” and “How to Act Now” as additional
themes. It has listed some tasks (see graphics) that are critical to
avoiding strokes.
Diabetologist V. Rajendran of Dr. Rajendran's Diabetes Centre says
diabetes mellitus by itself is one of the major and independent risk
factors for stroke. Large population studies have shown stroke to be
more frequent and have higher mortality in patients with diabetes, with
women being more prone to it.
The other associated risk factors increase this risk manifold. High
blood pressure and cholesterol and high-risk habits such as use of
tobacco and family history of stroke add to the risk that diabetes
already poses.
Diabetics should constantly monitor blood sugar level and also other
metabolic parameters such as cholesterol. Lifestyle and dietary changes
should be made if any of these are found to breach normal limits.
Hypertension
State president of Indian Medical Association L.P. Thangavel says people
are increasingly aware of stroke. Educated people also know that
uncontrolled hypertension and diabetes are major risk factors.
But, much needs to be done in the rural areas to increase awareness.
Hypertension and diabetes screening should be stepped up in rural areas
and those found with the symptoms should be educated on the risks from
the disease and how to avoid these.
Dr. Thangavel says the symptoms of stroke are easily understandable and
primary level physicians can identify these. With imaging systems such
as computed tomography available, detection is not a problem. Yet,
physicians must approach the patients showing the symptoms (see
graphics) with a high degree of suspicion so that accurate diagnosis is
not missed.
Brain gene activity changes through life
Studies track biochemical patterns from just after conception to old age
Human brains all work pretty much the same and use roughly the same
genes in the same way to build and maintain the infrastructure that
makes people who they are, two new studies show. And by charting the
brain’s genetic activity from before birth to old age, the studies
reveal that the brain continually remodels itself in predictable ways
throughout life.
In addition to uncovering details of how the brain grows and ages, the results may help scientists better understand what goes awry in brain disorders such as schizophrenia and autism.
“The complexity is mind-numbing,” says neuroscientist Stephen Ginsberg of the Nathan Kline Institute and New York University Langone Medical Center, who wasn’t involved in the studies. “It puts the brain in rarefied air.”
In the studies, published in the Oct. 27 Nature, researchers focused not on DNA — virtually every cell’s raw genetic material is identical — but on when, where and for how long each gene is turned on over the course of a person’s life. To do this, the researchers measured levels of mRNA, a molecule whose appearance marks one of the first steps in executing the orders contained in a gene, in postmortem samples of donated brains that ranged in age from weeks after conception to old age.
These different patterns of mRNA levels distinguish the brain from a heart, for instance, and a human from a mouse, too, says Nenad Šestan of Yale University School of Medicine and coauthor of one of the studies. “Essentially, we carry the same genes as mice,” he says. “However, in us, these genes are up to something quite different.”
To see what those genes were up to, Šestan’s study examined mRNA levels of different genes in 57 brain samples. The team divided the brain tissue up by region, so they were also able to get an idea of genes’ behavior in different parts of the brain. A parallel study, headed by Joel Kleinman of the National Institute of Mental Health in Bethesda, looked at gene behavior in 269 brain samples from a single region called the prefrontal cortex that also spanned the lifetime.
This approach allowed the researchers to get access to the brain that had previously been impossible.
“One of the limitations in studying human brain development is that you cannot do experiments,” Šestan says. “It’s very hard to understand when things happen.”
Both studies found lots of variation in gene behavior at different life stages, but one particular period stood out: The prenatal brain had massive changes in gene activity. Many genes there were pumping out big quantities of mRNA, and this production abruptly slowed after birth. “Prenatally, things are changing faster than they change at any other time,” says Carlo Colantuoni of the Lieber Institute for Brain Development at Johns Hopkins University Medical Center, and coauthor on one paper. “Things are happening fast in there.”
Kleinman and his colleagues turned up a curious finding: Many of the genes that slow down right after birth show a surge of activity as a person gets older. “The biggest changes that are going on occur fetally,” he says. “And then they drop off until mid-life, and then in the 50s to 70s, expression changes pick up again and become quite dramatic.”
Researchers don’t yet know what to make of this reversal, says Colantuoni. “We have just scratched the surface of what it means.”
Genes involved with building new brain cells were highly active early on, and then this activity quickly fell after birth. As these genes grew less active, genes involved in linking up nerve cells took on a greater role and became busier.
What’s more, the differences in gene behavior between male and female brains were greatest at early stages of development. Some of the genes found to be busier in male brains have been linked to schizophrenia, autism and other disorders that are known to be more prevalent among males, the researchers report. These disease-associated genes are very active early on in development and less so as a person ages, the researchers found, suggesting that something goes wrong very early in these conditions.
The scientists don’t know exactly which cells are responsible for these gene behavior differences. Figuring out whether gene behavior changes in all kinds of cells in the brain — neurons and glia, for instance — is the next step, says Ginsberg. “That’s going to be really important, especially for neuropsychiatric disorders.”
Although gene behavior is incredibly dynamic, the results suggest that brains are more alike than different. Despite millions of differences in DNA, brains have a common biochemical shape, Kleinman says. Two people who have very different DNA make-up don’t necessarily have very different gene behavior in the brain. “These individual genetic variations, they do matter — no question,” he says. But overall, genes behave similarly from person to person. “And that’s a really cool thing. It means that we’re much more alike than we are different.”
Many more studies are needed before scientists fully understand how the brain is built. Both teams plan on boosting the number of brain samples and studying the brains of people with disorders such as schizophrenia and autism. But the work is a major step forward, says geneticist Christopher Mason of Weill Cornell Medical College of Cornell University in New York City. “This is extraordinary work,” he says. “This is the beginning of telling us what the whole brain looks like.”
In addition to uncovering details of how the brain grows and ages, the results may help scientists better understand what goes awry in brain disorders such as schizophrenia and autism.
“The complexity is mind-numbing,” says neuroscientist Stephen Ginsberg of the Nathan Kline Institute and New York University Langone Medical Center, who wasn’t involved in the studies. “It puts the brain in rarefied air.”
In the studies, published in the Oct. 27 Nature, researchers focused not on DNA — virtually every cell’s raw genetic material is identical — but on when, where and for how long each gene is turned on over the course of a person’s life. To do this, the researchers measured levels of mRNA, a molecule whose appearance marks one of the first steps in executing the orders contained in a gene, in postmortem samples of donated brains that ranged in age from weeks after conception to old age.
These different patterns of mRNA levels distinguish the brain from a heart, for instance, and a human from a mouse, too, says Nenad Šestan of Yale University School of Medicine and coauthor of one of the studies. “Essentially, we carry the same genes as mice,” he says. “However, in us, these genes are up to something quite different.”
To see what those genes were up to, Šestan’s study examined mRNA levels of different genes in 57 brain samples. The team divided the brain tissue up by region, so they were also able to get an idea of genes’ behavior in different parts of the brain. A parallel study, headed by Joel Kleinman of the National Institute of Mental Health in Bethesda, looked at gene behavior in 269 brain samples from a single region called the prefrontal cortex that also spanned the lifetime.
This approach allowed the researchers to get access to the brain that had previously been impossible.
“One of the limitations in studying human brain development is that you cannot do experiments,” Šestan says. “It’s very hard to understand when things happen.”
Both studies found lots of variation in gene behavior at different life stages, but one particular period stood out: The prenatal brain had massive changes in gene activity. Many genes there were pumping out big quantities of mRNA, and this production abruptly slowed after birth. “Prenatally, things are changing faster than they change at any other time,” says Carlo Colantuoni of the Lieber Institute for Brain Development at Johns Hopkins University Medical Center, and coauthor on one paper. “Things are happening fast in there.”
Kleinman and his colleagues turned up a curious finding: Many of the genes that slow down right after birth show a surge of activity as a person gets older. “The biggest changes that are going on occur fetally,” he says. “And then they drop off until mid-life, and then in the 50s to 70s, expression changes pick up again and become quite dramatic.”
Researchers don’t yet know what to make of this reversal, says Colantuoni. “We have just scratched the surface of what it means.”
Genes involved with building new brain cells were highly active early on, and then this activity quickly fell after birth. As these genes grew less active, genes involved in linking up nerve cells took on a greater role and became busier.
What’s more, the differences in gene behavior between male and female brains were greatest at early stages of development. Some of the genes found to be busier in male brains have been linked to schizophrenia, autism and other disorders that are known to be more prevalent among males, the researchers report. These disease-associated genes are very active early on in development and less so as a person ages, the researchers found, suggesting that something goes wrong very early in these conditions.
The scientists don’t know exactly which cells are responsible for these gene behavior differences. Figuring out whether gene behavior changes in all kinds of cells in the brain — neurons and glia, for instance — is the next step, says Ginsberg. “That’s going to be really important, especially for neuropsychiatric disorders.”
Although gene behavior is incredibly dynamic, the results suggest that brains are more alike than different. Despite millions of differences in DNA, brains have a common biochemical shape, Kleinman says. Two people who have very different DNA make-up don’t necessarily have very different gene behavior in the brain. “These individual genetic variations, they do matter — no question,” he says. But overall, genes behave similarly from person to person. “And that’s a really cool thing. It means that we’re much more alike than we are different.”
Many more studies are needed before scientists fully understand how the brain is built. Both teams plan on boosting the number of brain samples and studying the brains of people with disorders such as schizophrenia and autism. But the work is a major step forward, says geneticist Christopher Mason of Weill Cornell Medical College of Cornell University in New York City. “This is extraordinary work,” he says. “This is the beginning of telling us what the whole brain looks like.”
Watching horror movies good for brain
Horror movies are good for mental health
Scared of watching horror flicks? Well, its bad news for the ladies who are wary of watching such movies.
Excuses for not watching the movies will not work anymore. Studies have shown that horror movies can be good for mental health and brain of women.
The benefit of watching scary movies proves that it has a positive effect on the mind, body and soul. Horror movies are not completely out of sync with reality. After all, it is the reality that creates fiction. So, watching such movies and relating with them is not a task at all. Thus, knowing it is fiction, a figment of imagination makes the audience sure that it is not real. Traumatic experiences after watching these horror and scary movies are rare because of this.
Research suggests that while women watch horror flicks, the brain secretes neurotransmitter dopamine, glutamate and serotonin. Thus, increased brain activity gets the state of mind alert for a while. Additionally , threat signals that pass through the hypothalamus (in the brain) will stimulate the adrenal glands to produce adrenaline and opiates which has an anesthesia like effect.
After watching the movie for half and hour, the system of the body will be calm and the defense system will become more powerful. That is when the immune system in the body will be stronger for a while.
So, no more excuses ladies. Watch horror flicks and be sure of having a positive effect on your mental health and body. Those who complain of heart complications should avoid watching such movies. Get ready, turn out the lights and watch some 'healthy' movies like Omen, The Exorcist and The exorcism of Emily Rose.
Excuses for not watching the movies will not work anymore. Studies have shown that horror movies can be good for mental health and brain of women.
The benefit of watching scary movies proves that it has a positive effect on the mind, body and soul. Horror movies are not completely out of sync with reality. After all, it is the reality that creates fiction. So, watching such movies and relating with them is not a task at all. Thus, knowing it is fiction, a figment of imagination makes the audience sure that it is not real. Traumatic experiences after watching these horror and scary movies are rare because of this.
Research suggests that while women watch horror flicks, the brain secretes neurotransmitter dopamine, glutamate and serotonin. Thus, increased brain activity gets the state of mind alert for a while. Additionally , threat signals that pass through the hypothalamus (in the brain) will stimulate the adrenal glands to produce adrenaline and opiates which has an anesthesia like effect.
After watching the movie for half and hour, the system of the body will be calm and the defense system will become more powerful. That is when the immune system in the body will be stronger for a while.
So, no more excuses ladies. Watch horror flicks and be sure of having a positive effect on your mental health and body. Those who complain of heart complications should avoid watching such movies. Get ready, turn out the lights and watch some 'healthy' movies like Omen, The Exorcist and The exorcism of Emily Rose.
Brain Transcriptome Reveals Gender-Biased Gene Expression
Trajectories of genes identified which are linked to neurobiological categories and diseases
FRIDAY, Oct. 28 (HealthDay News) -- Generation and analysis of an exon-level transcriptome of the human brain and associated genotyping data shows that the transcriptome is organized into different coexpression networks, and shows gender-biased gene expression and exon usage, according to a study published in the Oct. 27 issue of Nature.
Hyo Jung Kang, Ph.D., from the Yale University School of Medicine in New Haven, Conn., and colleagues investigated the exon-level transcriptome and associated genotyping data, for males and females of different ethnicities, from multiple brain regions and neocortical areas of developing and adult postmortem human brains. A total of 1,340 tissue samples taken from 57 subjects, aged from 40 days after conception to 82 years, were analyzed.
The investigators found that 86 percent of the genes assessed were expressed. Of these, 90 percent were differentially regulated at the whole-transcript or exon level across brain regions and/or over time. Most of the regional and temporal differences were identified before birth; subsequent increases in the similarity were among regional transcriptomes. The brain transcriptome shows gender-biased gene expression and exon usage, and is organized into discrete coexpression networks. Trajectories of genes linked to neurobiological categories and diseases were found, and correlations were identified between single nucleotide polymorphisms and gene expression.
Dopamine release in human brain tracked at microsecond timescale reveals decision-making
A research team led by investigators at the Virginia Tech Carilion
Research Institute has demonstrated the first rapid measurements of
dopamine release in a human brain and provided preliminary evidence that
the neurotransmitter can be tracked in its movement between brain cells
while a subject expresses decision-making behavior.
"In an experiment where we measured dopamine release while a subject made investment decisions in a stock market trading game, we showed that dopamine tracks changes in the value of the market," said Read Montague, director of the Human Neuroimaging Laboratory at the Virginia Tech Carilion Research Institute and professor of physics in the College of Science at Virginia Tech.
"A startling discovery was that the dopamine signal appeared to be a very good indicator of the market value and in many instances a good predictor of future market changes," said Kenneth Kishida, a postdoctoral associate with the Human Neuroimaging Laboratory and the lead author on the report. Interestingly, the choice expressed by the subject did not always correspond with the prescient brain chemistry, he said.
The research was published on Aug. 4, 2011, in the Public Library of Science journal, PLoS ONE, in the article "Sub-Second Dopamine Detection in Human Striatum," by Kishida; Stefan G. Sandberg, senior fellow with the Departments of Psychiatry and Behavioral Sciences and Pharmacology, University of Washington, Seattle; Terry Lohrenz, assistant professor in the Department of Neuroscience, Baylor College of Medicine; Dr. Youssef G. Comair, professor and chief, Division of Neurosurgery, American University of Beirut, Lebanon; Ignacio Saez, assistant professor at Virginia Tech Carilion Research Institute; Paul E. M. Phillips, associate professor, Departments of Psychiatry and Behavioral Sciences and Pharmacology, University of Washington, Seattle; and Montague, senior author.
The researchers adapted their sensors to existing technology used for functional mapping of the brain during surgical implantation of deep-brain stimulation devices. "Deep-brain stimulation is typically used in the treatment of Parkinson's disease," said Montague. "Uses for treating other neurological disorders are also being investigated, though, and may open new avenues for the technology we developed."
The researchers applied criteria that employed experimental methodology that is "safe to the patient, compatible with existing neurosurgical apparatus and the operating-room environment, and capable of sub-second detection of physiological dopamine," they state in the article. They modified existing sensor technology to improve signal conductivity, creating a microsensor that shares the electrochemical properties of existing electrodes yet can detect sub-second dopamine release. "Even more important, the new microsensors are biocompatible and can be sterilized without affecting performance, " Kishida added.
The new instrument was demonstrated in a single human subject, a consenting patient with late-stage Parkinson's disease who was undergoing elective surgery for deep-brain stimulation electrode implantation.
The new microsensor was placed in the patient's brain and dopamine release was monitored as the patient engaged in a decision-making game. The current value and recent history of a stock market was graphically represented on a laptop monitor. The subject chose the proportion of a portfolio initially valued at $100 to be invested in the stock market. Decisions were submitted by pushing buttons on handheld response devices. Following the submission of each decision, the market was updated. The final portfolio determined the actual payout at the end of the experiment.
The researchers report that they were surprised to observe that "the slope of the dopamine signal over a period five seconds prior to a market price update correlated with subsequent market returns…, demonstrating that it is a significant predictor of future market activity."
To test this hypothesis, the researchers constructed a trader model that made decisions based on the fluctuations in the dopamine signal leading up to the market price changes. This decision model invested 100 percent, or all in, when the dopamine slope was positive and 0 percent, or all out, when the slope was negative. The researchers report that, "Over the five markets played, this trader model earned 202 points (a gain of 175 percent), more than two times the amount earned by the subject's expressed behavior. These data demonstrate that the information encoded in the dopamine signal of this patient is potentially useful for economic decision making."
"This exciting preliminary result requires replication, but it immediately sets the imagination in motion," said Kishida. "I often wonder whether there is a feeling associated with these dopamine fluctuations and whether there is any connection with that 'gut feeling' people sometimes ignore."
Writing in the PLoS ONE article, the researchers conclude, "This methodological demonstration opens the door to future investigations utilizing sub-second chemical measurements in the human brain, which should yield important insights into the role of dopamine signaling in human decision-making."
"In an experiment where we measured dopamine release while a subject made investment decisions in a stock market trading game, we showed that dopamine tracks changes in the value of the market," said Read Montague, director of the Human Neuroimaging Laboratory at the Virginia Tech Carilion Research Institute and professor of physics in the College of Science at Virginia Tech.
"A startling discovery was that the dopamine signal appeared to be a very good indicator of the market value and in many instances a good predictor of future market changes," said Kenneth Kishida, a postdoctoral associate with the Human Neuroimaging Laboratory and the lead author on the report. Interestingly, the choice expressed by the subject did not always correspond with the prescient brain chemistry, he said.
The research was published on Aug. 4, 2011, in the Public Library of Science journal, PLoS ONE, in the article "Sub-Second Dopamine Detection in Human Striatum," by Kishida; Stefan G. Sandberg, senior fellow with the Departments of Psychiatry and Behavioral Sciences and Pharmacology, University of Washington, Seattle; Terry Lohrenz, assistant professor in the Department of Neuroscience, Baylor College of Medicine; Dr. Youssef G. Comair, professor and chief, Division of Neurosurgery, American University of Beirut, Lebanon; Ignacio Saez, assistant professor at Virginia Tech Carilion Research Institute; Paul E. M. Phillips, associate professor, Departments of Psychiatry and Behavioral Sciences and Pharmacology, University of Washington, Seattle; and Montague, senior author.
The researchers adapted their sensors to existing technology used for functional mapping of the brain during surgical implantation of deep-brain stimulation devices. "Deep-brain stimulation is typically used in the treatment of Parkinson's disease," said Montague. "Uses for treating other neurological disorders are also being investigated, though, and may open new avenues for the technology we developed."
The researchers applied criteria that employed experimental methodology that is "safe to the patient, compatible with existing neurosurgical apparatus and the operating-room environment, and capable of sub-second detection of physiological dopamine," they state in the article. They modified existing sensor technology to improve signal conductivity, creating a microsensor that shares the electrochemical properties of existing electrodes yet can detect sub-second dopamine release. "Even more important, the new microsensors are biocompatible and can be sterilized without affecting performance, " Kishida added.
The new instrument was demonstrated in a single human subject, a consenting patient with late-stage Parkinson's disease who was undergoing elective surgery for deep-brain stimulation electrode implantation.
The new microsensor was placed in the patient's brain and dopamine release was monitored as the patient engaged in a decision-making game. The current value and recent history of a stock market was graphically represented on a laptop monitor. The subject chose the proportion of a portfolio initially valued at $100 to be invested in the stock market. Decisions were submitted by pushing buttons on handheld response devices. Following the submission of each decision, the market was updated. The final portfolio determined the actual payout at the end of the experiment.
The researchers report that they were surprised to observe that "the slope of the dopamine signal over a period five seconds prior to a market price update correlated with subsequent market returns…, demonstrating that it is a significant predictor of future market activity."
To test this hypothesis, the researchers constructed a trader model that made decisions based on the fluctuations in the dopamine signal leading up to the market price changes. This decision model invested 100 percent, or all in, when the dopamine slope was positive and 0 percent, or all out, when the slope was negative. The researchers report that, "Over the five markets played, this trader model earned 202 points (a gain of 175 percent), more than two times the amount earned by the subject's expressed behavior. These data demonstrate that the information encoded in the dopamine signal of this patient is potentially useful for economic decision making."
"This exciting preliminary result requires replication, but it immediately sets the imagination in motion," said Kishida. "I often wonder whether there is a feeling associated with these dopamine fluctuations and whether there is any connection with that 'gut feeling' people sometimes ignore."
Writing in the PLoS ONE article, the researchers conclude, "This methodological demonstration opens the door to future investigations utilizing sub-second chemical measurements in the human brain, which should yield important insights into the role of dopamine signaling in human decision-making."
Genetic Regulation of Brain Development Implicated in Mental Illness
A
major study of the genes associated with psychiatric illnesses has
discovered that most of the genes are in place before birth in the
developing human brain.Yale University researchers also discovered that hundreds of genetic differences were found between males and females as their brains take shape in the womb.
The study is found in the journal Nature.
Neuroscientists estimate the human brain has a hundred billion brain cells requiring an incalculable number of connections.
In the study, Yale researchers tracked 86 percent of 17,000 human genes that are believed to be recruited in the effort to create the brain.
Investigators studied not only what genes are involved in development, but where and when they are expressed, or activated.
“We knew many of the genes involved in the development of the brain, but now we know where and when they are functioning in the human brain,” said Nenad Sestan, M.D., Ph.D., senior author of the study.
“The complexity of the system shows why the human brain may be so susceptible to psychiatric disorders.”
The study identified genes represented in the human brain, and when and where in the brain they were expressed. Scientists used more than 1,300 tissue samples taken from 57 subjects, aged from 40 days after conception to 82 years.
The analysis of over 1.9 billion data points by the Yale scientists created an unprecedented map of genetic activity in the brain at different stages of development.
Researchers were impressed to find much of the human brain is shaped prior to birth.
For instance, the team analyzed genes and variants previously linked with autism and schizophrenia, the symptoms of which are evident in the first few years of life or during early adulthood, respectively. The new analysis shows molecular evidence of expression of these suspect genes prior to birth.
“We found a distinct pattern of gene expression and variations prenatally in areas of the brain involving higher cognitive function,” Sestan said. “It is clear that these disease-associated genes are developmentally regulated.”
When comparing the brains of men and women, researchers noticed that in addition to the Y chromosome gene found in only in men, each gender presents distinct differences in many of genes that are shared by both sexes.
This difference was noted both for when the gene was expressed and the level of the gene’s activity. Most of the differences were noted prenatally.
Galloping ganglia: Random Dance studies the brain
McGregor, whose company, Random Dance, returned to the Peak Performances series at Montclair State University, on Thursday, has a similar problem. He, too, is engaged in scientific research—cognitive studies that help latter-day investigators understand how the brain makes decisions. McGregor says that participating in these studies gives him and his dancers fresh ideas for how to proceed.
Yet something is missing from “Far,” the glamorous contemporary work making its local premiere. The ghost, in this case, is the choreographer himself—the agent who must tie the fractured movements and the segments of the show together. Though continuously surprising, the piece remains unsatisfying because McGregor does not allow us to glimpse the animating intelligence behind it. The choreographer is always our stand-in for God, but this one seems so concerned with creating new material that as it emerges, he forgets to shape it into a Divine Plan. He prefers flow to structure.
In every other respect, “Far” is stunning. McGregor’s dancers are sleek and shapely, moving with fluid assurance, and above the stage hangs a dazzling object: a rectangular LED display that continually changes appearance, generating new patterns of light and shadow by responding to stimuli. Shining promiscuously like a galaxy or retreating to a single glowing point, this machine is the evening’s star performer, and lighting designer Lucy Carter amplifies its effects with tinted clouds of smoke. Ben Frost’s episodic sound score ranges widely, from Vivaldi to the sound of animals grunting.
The piece opens with a striking image: Daniela Neugebauer standing center stage flanked by women torch-bearers, with Paolo Mangiola regarding her from a shadowy vantage off to the side. She seems inclined to ignore him, but after a quick pass to get a closer look, he insists upon engaging her in a duet that sets the tone for difficult relationships between men and women. Adjusting his grip, suddenly his hands are at her throat. Yet at another point, after shrugging him off she turns and offers her hand. Eventually they seem to reach a cool accord, lying parallel to each other.
A series of solos follows, with hinged movement that tends to emphasize a particular body part—first shoulders, and then ribs. Quick, struggling encounters characterize a group section, and later, in a bit of pantomime that stands out for its naturalness, Anna Nowak chats with Mangiola trying to put him off. He responds by seizing her wrists.
A male duet seems less coercive. Although it ends before both parties are quite ready, they salute each other with a courtly bow.
The final duet is the tenderest yet. Catarina Carvalho has the space to swivel in Alexander Whitley’s loose embrace, and she willingly hangs on his back with her hands pressed to his chest. Yet this freedom, too, seems like the prelude to a departure. She fades and lies still. He watches for a moment, and then turns to leave.
Saturday, October 15, 2011
Differing structures underlie differing brain rhythms in healthy and ill
Virtual brains modeling epilepsy and schizophrenia display less
complexity among functional connections, and other differences compared
to healthy brain models, researchers at Case Western Reserve University
School of Medicine report.
The researchers worked backward from brain rhythms – the oscillating patterns of electrical activity in the brain recorded on electroencephalograms - from both healthy and ill individuals.
These oscillations relate to the state of awareness. But, instead of seeking answers to how the rhythms emerge, the investigators built models that, when they reproduced the different neural activity patterns seen in real brains, revealed underlying structural differences among the healthy and ill.
Their work is published in the online journal PLoS Computational Biology.
"Our hypothesis is that healthy brains share features with the virtual healthy brains and unhealthy brains share features with virtual unhealthy brains," said Roberto Fernández Galán, a professor of neurosciences at Case Western Reserve School of Medicine. Galán has a background in physics, electrophysiology and computational neuroscience.
Galán worked with G. Karl Steinke, a former graduate student in Biomedical Engineering at Case School of Engineering, and now a researcher at Boston Scientific Neroumodulation.
After breaking down the oscillating patterns of brain activity collected from real EEGs and MEGs into a usable form, the researchers applied inverse calculations and reverse engineering to develop brain models they refer to as virtual brains.
The most striking difference they found is in the hierarchical networks of brain connections among the models of healthy and unhealthy brains, Galán said. "The more complex the network, the more normal the EEG pattern."
"A healthy brain network is similar to the airport network," he explained. "There are a small number of hubs with many connections to other airports and a large number of smaller airports with only a few connections." In the brain model, the airports are called nodes and in the healthy model, about 10 percent of nodes are hubs.
In the real brain, the prefrontal cortex, which is a center for complex thought, social behavior and more, is a hub. "It is thus reasonable to think that the functional connectivity of the prefrontal cortex is altered in pathologies like schizophrenia", said Galán.
Indeed, the network in the epileptic brain model is less complex than the healthy model and the network in the schizophrenia model is even less so. The result is that the dominance of the hubs falls off, which may be indicative of a neuropathology or mental illness, the researchers say.
Their analysis reveals that oscillating brain activity in the virtual models appear to emerge from interactions among neurons and not from so-called pacemakers, which some researchers hypothesize are specialized neurons generating different rhythms of activity in the brain.
This information, combined with finding that healthy brain rhythms are not homogeneously distributed across all virtual brain nodes, supports the idea that oscillations may be a mechanism linking perceptual information across sensory and associative areas of the brain, the researchers say.
Galán and Steinke also discovered that nodes receiving the greatest input produced the smallest fluctuations in activity in the healthy and epileptic brain models. But the inverse relationship was not seen in the schizophrenic model.
The researchers have made the computer programs that run their algorithms and simulations available free to clinicians and other investigators who want to test the predictions made by the models or to expand their own studies. They are included in the supplemental materials, along with technical instructions supplied with the paper or at http://www.case.edu/med/galanlab/software.html.
The research was funded through grants from the Mt. Sinai Foundation
and the Alfred P. Sloan Foundation awarded to Galán and through a
Choose Ohio First grant awarded to Steinke. The brain models were
simulated and analyzed in part using the High Performance Computing
Cluster at Case Western Reserve University.
The researchers worked backward from brain rhythms – the oscillating patterns of electrical activity in the brain recorded on electroencephalograms - from both healthy and ill individuals.
These oscillations relate to the state of awareness. But, instead of seeking answers to how the rhythms emerge, the investigators built models that, when they reproduced the different neural activity patterns seen in real brains, revealed underlying structural differences among the healthy and ill.
Their work is published in the online journal PLoS Computational Biology.
"Our hypothesis is that healthy brains share features with the virtual healthy brains and unhealthy brains share features with virtual unhealthy brains," said Roberto Fernández Galán, a professor of neurosciences at Case Western Reserve School of Medicine. Galán has a background in physics, electrophysiology and computational neuroscience.
Galán worked with G. Karl Steinke, a former graduate student in Biomedical Engineering at Case School of Engineering, and now a researcher at Boston Scientific Neroumodulation.
After breaking down the oscillating patterns of brain activity collected from real EEGs and MEGs into a usable form, the researchers applied inverse calculations and reverse engineering to develop brain models they refer to as virtual brains.
The most striking difference they found is in the hierarchical networks of brain connections among the models of healthy and unhealthy brains, Galán said. "The more complex the network, the more normal the EEG pattern."
"A healthy brain network is similar to the airport network," he explained. "There are a small number of hubs with many connections to other airports and a large number of smaller airports with only a few connections." In the brain model, the airports are called nodes and in the healthy model, about 10 percent of nodes are hubs.
In the real brain, the prefrontal cortex, which is a center for complex thought, social behavior and more, is a hub. "It is thus reasonable to think that the functional connectivity of the prefrontal cortex is altered in pathologies like schizophrenia", said Galán.
Indeed, the network in the epileptic brain model is less complex than the healthy model and the network in the schizophrenia model is even less so. The result is that the dominance of the hubs falls off, which may be indicative of a neuropathology or mental illness, the researchers say.
Their analysis reveals that oscillating brain activity in the virtual models appear to emerge from interactions among neurons and not from so-called pacemakers, which some researchers hypothesize are specialized neurons generating different rhythms of activity in the brain.
This information, combined with finding that healthy brain rhythms are not homogeneously distributed across all virtual brain nodes, supports the idea that oscillations may be a mechanism linking perceptual information across sensory and associative areas of the brain, the researchers say.
Galán and Steinke also discovered that nodes receiving the greatest input produced the smallest fluctuations in activity in the healthy and epileptic brain models. But the inverse relationship was not seen in the schizophrenic model.
The researchers have made the computer programs that run their algorithms and simulations available free to clinicians and other investigators who want to test the predictions made by the models or to expand their own studies. They are included in the supplemental materials, along with technical instructions supplied with the paper or at http://www.case.edu/med/galanlab/software.html.
Foundation Aims to Raise Awareness of Brain Diseases
American Academy of Neurology Foundation marks 20th anniversary with call for research support
One in six people in the United States is affected by a brain disease such as stroke, dementia, epilepsy or multiple sclerosis, and more research is required to find new treatments, says the American Academy of Neurology Foundation. To mark its 20th anniversary, the foundation has released a video public service announcement to raise awareness about the need for ongoing research."Brain disease is in the news every day, and it is nearly impossible to find someone who has not had a family member or friend affected by one of the many forms of brain disease that attack the brain and nervous system," Dr. John Mazziotta, chair of the foundation's board of trustees and professor and chair of the Brain Mapping Center at the University of California, Los Angeles, said in an AAN news release.
"People are also concerned they, or their family members, will become affected by brain disease directly," he added.
The new public service announcement, posted on YouTube, was created using clips from some of the more than 100 accepted entries into the 2011 Neuro Film Festival. The annual contest is hosted by the foundation and features videos from people affected by brain disease.
"There is vast research potential for finding new treatments for brain disease, but limited funding to support it," Mazziotta said.
According to the news release, the foundation, which supports research into finding cures for brain diseases, has raised more than $16 million to fund such efforts to help battle stroke (the third leading cause of death in the United States) and Alzheimer's disease (the sixth leading cause of death in the country).
Gantenerumab Reduces Brain Amyloid in Alzheimer's
Treatment with gantenerumab, an anti–amyloid-β
monoclonal antibody, resulted in a dose-dependent reduction in brain
amyloid in patients with mild to moderate Alzheimer's disease (AD), a
small trial shows.
However, "no consistent treatment effects on cognitive measures were noted in this small group of patients treated for a short period of time," wrote lead author Susanne Ostrowitzki, MD, who works in the Department of Neuroscience at F. Hoffmann-La Roche Ltd. — the drug’s manufacturer — in Basel, Switzerland.
"It is still unclear whether any reduction in brain amyloid level will translate into clinical efficacy."
Findings from the study, funded by the company, were reported online October 10 in the Archives of Neurology.
Passive Immunotherapy
"This kind of antibody treatment is considered passive immunotherapy and is in contrast to active immunotherapy or vaccination where the body’s immune system is activated in response to the vaccine to produce antibodies," explained senior author Luca Santarelli, MD, also with the company, in an email to Medscape Medical News.
"Administering gantenerumab circumvents stimulation of the adaptive immune system and ensures adequate antibody exposure in the Alzheimer’s patient."
The study included data from 16 AD patients, aged 50 to 90 years, who were included in a positron emission tomographic (PET) substudy of a larger multiple ascending dose trial.
For inclusion in the study the patients must have probable AD according to the National Institute of Neurological Disorders and Stroke – Alzheimer’s Disease and Related Disorders Association criteria, a Mini-Mental State Examination Score between 16 and 26 (inclusive), a magnetic resonance imaging (MRI) scan consistent with AD, and a modified Hachinski ischemia score of 4 or less.
APOE genotyping was performed for all patients.
The patients were assigned to receive intravenous infusions of gantenerumab (60 mg, n = 6; 200 mg, n = 6) or placebo (n = 4) once every 4 weeks to a total of 7 infusions, but because of early termination of dosing in the 200-mg gantenerumab group, not all participants received 7 infusions.
In the 60-mg group, all patients received 7 infusions, while in the 200-mg group 1 patient received 5 infusions, 2 patients received 4 infusions, 2 patients received 3 infusions, and 1 patient received 2 infusions.
In the placebo group, 2 patients received all 7 infusions, 1 patient received 5 infusions, and 1 patient received 2 infusions.
Baseline images were compared with images obtained at the end of treatment to determine the change in brain amyloid, as measured by carbon 11-labeled Pittsburgh compound B PET.
Additionally, to evaluate gantenerumab’s ability to clear amyloid plaques via phagocytosis, primary microglial cells obtained from healthy human brain tissue during tumor surgery were incubated in different concentrations of the drug.
The study found a mean percentage reduction from baseline in cortical brain amyloid relative to placebo of 15.6% in the 60-mg group and 35.7% in the 200-mg group.
Findings in the placebo group support previous reports that "amyloid load continues to increase in many patients with mild-to-moderate AD," the authors added.
Microhemorrhage
Two patients treated with gantenerumab, both of them APOE ε4 homozygous, showed abnormalities on MRI fluid-attenuated inversion recovery (FLAIR) imaging that were "consistent with inflammation or vasogenic edema" after 2 and 4 of the 200-mg doses.
Both patients also developed microhemorrhages, and 1 was "mildly symptomatic" with headaches, dizziness, gait instability, and tremor, the investigators reported.
These adverse effects resolved spontaneously after discontinuation of dosing, similar to what has been reported after treatment with bapineuzumab, they noted.
The FLAIR abnormalities were most conspicuous in areas of more prominent amyloid reduction and "may be seen as instances of excessive pharmacological activity due to a high dose or more susceptible individuals (e.g., carriers of the APOE ε4 genotype)," they wrote.
However, according to the researchers, a smaller reduction in amyloid was seen with no FLAIR abnormalities at a lower dose of gantenerumab.
"This suggests that gantenerumab-induced amyloid lowering can be achieved without significantly perturbing vascular permeability through inflammation or blockage of Aβ clearance pathways when appropriate dosing is selected."
"As with any drug, it is critically important to identify a dose or doses, with the best risk benefit ratio," Dr. Santarelli told Medscape Medical News. "The imaging data suggest that such a dose that results in brain amyloid reduction, yet is well tolerated and does not lead to changes on MR scans, may be identified."
Combined with the ex vivo results showing gantenerumab-induced phagocytosis of amyloid in a dose-dependent fashion, the study’s findings support the hypothesis that the mechanism by which gantenerumab clears amyloid plaques is "via Fc receptor/microglia-mediated phagocytosis," the authors suggested.
"A phase 2 clinical trial is underway to investigate whether a clinical benefit can be achieved with gantenerumab-treated patients," they conclude.
Other Antibody Strategies
Asked for comment on these findings, Rachelle S. Doody, MD, PhD, director of the Alzheimer's Disease and Memory Disorders Center at Baylor College of Medicine in Houston, Texas, pointed out that "there are at least seven other antibody-related infusion treatments under development and in human stages of testing, and none of them have so far been proven to benefit patients clinically."
"We must await data from larger studies designed and powered to look at efficacy," she told Medscape Medical News.
Although amyloid reduction was "notable and statistically significant" among participants receiving the higher dose of gantenerumab, there was only a marginal effect in those receiving the lower dose, she noted.
However, in this latter group, amyloid "did not increase as much as it did for placebo treated patients, and this difference was also statistically significant."
Changes such as edema or microhemorrhage in the brain are always concerning, she added.
"In other antibody studies we have seen that such changes can often be asymptomatic, or can be associated with stroke-like symptoms. So there may be a need to monitor patients with MRI scans if these therapies are proven to be effective. The hope is that these side effects of therapy will be manageable by altering or delaying the dose of antibodies."
The study was funded by F. Hoffmann-La Roche Ltd. Eight of the 12 study authors, including Dr. Ostrowitzki and Dr. Santarelli, are full-time employees of Roche/F. Hoffmann-La Roche Ltd, and they may additionally hold Roche stock/stock options. Dr. Thurfjell is a full-time employee of GE Healthcare, and Dr. Brooks holds a part-time position as a senior neurologist with GE Healthcare, which holds a license agreement with the University of Pittsburgh based on the [11C]PiB PET technology described in this study. During the past 12 months, Dr. Brooks has also received consultancy fees from Synosia, Schering Plough, Amsterdam Molecular Therapeutics, Biogen Idec, NeuroNova, Shire, Genentech, and Janssen and honoraria from Teva, UCB, GlaxoSmithKline, and Orion Pharma. Dr. Barkhof is receiving consultancy fees from pharmaceutical companies, including F. Hoffmann-La Roche Ltd. Dr. Klunk is the co-inventor of this technology and, as such, has a financial interest in this license agreement. GE Healthcare has provided grant support and consultant fees to Dr. Klunk for studies unrelated to this work, and Dr. Klunk has received consultant fees/honoraria related to this study from Roche. Dr. Doody disclosed that her group is involved in the development of proteomic biological markers through the state-funded Texas Alzheimer's Disease Research and Care Consortium; her institution receives support from the National Institutes of Health for the Alzheimer's Disease Neuroimaging Initiative, for which she serves as the local principal investigator and on the national steering committee; and she has provided ad hoc consultation to six of the seven companies involved in the development of passive immunization therapies, including F. Hoffmann-La Roche Ltd.
However, "no consistent treatment effects on cognitive measures were noted in this small group of patients treated for a short period of time," wrote lead author Susanne Ostrowitzki, MD, who works in the Department of Neuroscience at F. Hoffmann-La Roche Ltd. — the drug’s manufacturer — in Basel, Switzerland.
"It is still unclear whether any reduction in brain amyloid level will translate into clinical efficacy."
Findings from the study, funded by the company, were reported online October 10 in the Archives of Neurology.
Passive Immunotherapy
"This kind of antibody treatment is considered passive immunotherapy and is in contrast to active immunotherapy or vaccination where the body’s immune system is activated in response to the vaccine to produce antibodies," explained senior author Luca Santarelli, MD, also with the company, in an email to Medscape Medical News.
"Administering gantenerumab circumvents stimulation of the adaptive immune system and ensures adequate antibody exposure in the Alzheimer’s patient."
The study included data from 16 AD patients, aged 50 to 90 years, who were included in a positron emission tomographic (PET) substudy of a larger multiple ascending dose trial.
For inclusion in the study the patients must have probable AD according to the National Institute of Neurological Disorders and Stroke – Alzheimer’s Disease and Related Disorders Association criteria, a Mini-Mental State Examination Score between 16 and 26 (inclusive), a magnetic resonance imaging (MRI) scan consistent with AD, and a modified Hachinski ischemia score of 4 or less.
APOE genotyping was performed for all patients.
The patients were assigned to receive intravenous infusions of gantenerumab (60 mg, n = 6; 200 mg, n = 6) or placebo (n = 4) once every 4 weeks to a total of 7 infusions, but because of early termination of dosing in the 200-mg gantenerumab group, not all participants received 7 infusions.
In the 60-mg group, all patients received 7 infusions, while in the 200-mg group 1 patient received 5 infusions, 2 patients received 4 infusions, 2 patients received 3 infusions, and 1 patient received 2 infusions.
In the placebo group, 2 patients received all 7 infusions, 1 patient received 5 infusions, and 1 patient received 2 infusions.
Baseline images were compared with images obtained at the end of treatment to determine the change in brain amyloid, as measured by carbon 11-labeled Pittsburgh compound B PET.
Additionally, to evaluate gantenerumab’s ability to clear amyloid plaques via phagocytosis, primary microglial cells obtained from healthy human brain tissue during tumor surgery were incubated in different concentrations of the drug.
The study found a mean percentage reduction from baseline in cortical brain amyloid relative to placebo of 15.6% in the 60-mg group and 35.7% in the 200-mg group.
Findings in the placebo group support previous reports that "amyloid load continues to increase in many patients with mild-to-moderate AD," the authors added.
Microhemorrhage
Two patients treated with gantenerumab, both of them APOE ε4 homozygous, showed abnormalities on MRI fluid-attenuated inversion recovery (FLAIR) imaging that were "consistent with inflammation or vasogenic edema" after 2 and 4 of the 200-mg doses.
Both patients also developed microhemorrhages, and 1 was "mildly symptomatic" with headaches, dizziness, gait instability, and tremor, the investigators reported.
These adverse effects resolved spontaneously after discontinuation of dosing, similar to what has been reported after treatment with bapineuzumab, they noted.
The FLAIR abnormalities were most conspicuous in areas of more prominent amyloid reduction and "may be seen as instances of excessive pharmacological activity due to a high dose or more susceptible individuals (e.g., carriers of the APOE ε4 genotype)," they wrote.
However, according to the researchers, a smaller reduction in amyloid was seen with no FLAIR abnormalities at a lower dose of gantenerumab.
"This suggests that gantenerumab-induced amyloid lowering can be achieved without significantly perturbing vascular permeability through inflammation or blockage of Aβ clearance pathways when appropriate dosing is selected."
"As with any drug, it is critically important to identify a dose or doses, with the best risk benefit ratio," Dr. Santarelli told Medscape Medical News. "The imaging data suggest that such a dose that results in brain amyloid reduction, yet is well tolerated and does not lead to changes on MR scans, may be identified."
Combined with the ex vivo results showing gantenerumab-induced phagocytosis of amyloid in a dose-dependent fashion, the study’s findings support the hypothesis that the mechanism by which gantenerumab clears amyloid plaques is "via Fc receptor/microglia-mediated phagocytosis," the authors suggested.
"A phase 2 clinical trial is underway to investigate whether a clinical benefit can be achieved with gantenerumab-treated patients," they conclude.
Other Antibody Strategies
Asked for comment on these findings, Rachelle S. Doody, MD, PhD, director of the Alzheimer's Disease and Memory Disorders Center at Baylor College of Medicine in Houston, Texas, pointed out that "there are at least seven other antibody-related infusion treatments under development and in human stages of testing, and none of them have so far been proven to benefit patients clinically."
"We must await data from larger studies designed and powered to look at efficacy," she told Medscape Medical News.
Although amyloid reduction was "notable and statistically significant" among participants receiving the higher dose of gantenerumab, there was only a marginal effect in those receiving the lower dose, she noted.
However, in this latter group, amyloid "did not increase as much as it did for placebo treated patients, and this difference was also statistically significant."
Changes such as edema or microhemorrhage in the brain are always concerning, she added.
"In other antibody studies we have seen that such changes can often be asymptomatic, or can be associated with stroke-like symptoms. So there may be a need to monitor patients with MRI scans if these therapies are proven to be effective. The hope is that these side effects of therapy will be manageable by altering or delaying the dose of antibodies."
The study was funded by F. Hoffmann-La Roche Ltd. Eight of the 12 study authors, including Dr. Ostrowitzki and Dr. Santarelli, are full-time employees of Roche/F. Hoffmann-La Roche Ltd, and they may additionally hold Roche stock/stock options. Dr. Thurfjell is a full-time employee of GE Healthcare, and Dr. Brooks holds a part-time position as a senior neurologist with GE Healthcare, which holds a license agreement with the University of Pittsburgh based on the [11C]PiB PET technology described in this study. During the past 12 months, Dr. Brooks has also received consultancy fees from Synosia, Schering Plough, Amsterdam Molecular Therapeutics, Biogen Idec, NeuroNova, Shire, Genentech, and Janssen and honoraria from Teva, UCB, GlaxoSmithKline, and Orion Pharma. Dr. Barkhof is receiving consultancy fees from pharmaceutical companies, including F. Hoffmann-La Roche Ltd. Dr. Klunk is the co-inventor of this technology and, as such, has a financial interest in this license agreement. GE Healthcare has provided grant support and consultant fees to Dr. Klunk for studies unrelated to this work, and Dr. Klunk has received consultant fees/honoraria related to this study from Roche. Dr. Doody disclosed that her group is involved in the development of proteomic biological markers through the state-funded Texas Alzheimer's Disease Research and Care Consortium; her institution receives support from the National Institutes of Health for the Alzheimer's Disease Neuroimaging Initiative, for which she serves as the local principal investigator and on the national steering committee; and she has provided ad hoc consultation to six of the seven companies involved in the development of passive immunization therapies, including F. Hoffmann-La Roche Ltd.
Do ADHD Drugs Boost Dopamine Levels?
Brain
scans may become an effective way of testing whether a drug designed
for attention-deficit disorder can raise dopamine levels, according to
research at the Washington University School of Medicine in St. Louis.In a previous mouse study, the same group discovered that by raising dopamine levels they could improve attention problems caused by neurofibromatosis type 1 (NF1), a disorder that affects more than 100,000 people in the United States. About 60 to 80 percent of children with NF1 have some sort of attention deficit.
“Many kids with NF1 really struggle in school, and finding ways to help alleviate attention problems is a high priority,” says David H. Gutmann, MD, PhD and Donald O. Schnuck Family Professor of Neurology. “The technique we’ve refined may make it possible to match specific treatments to the patients with NF1 and attention deficit who are most likely to benefit from those treatments.”
Symptoms of NF1 attention deficits are similar to other types of attention deficit disorders. It’s unclear, however, whether the brain differences that trigger these issues in children with NF1 are the same brain changes that underlie attention deficits in the general population.
“This mouse model may not be a perfect model for all forms of attention deficit, but it is a terrific model for one type of attention system dysfunction,” Gutmann says. “Greater understanding of what goes wrong in some children with NF1 could lead to new insights into a broader variety of attention problems.”
Gutmann, director of the Washington University Neurofibromatosis (NF) Center, and his team genetically engineered mice to develop NF1 attention problems and brain tumors.
Last year, Gutmann demonstrated that one of these strands of mice had lower levels of dopamine in part of the brain. After treating these mice with Ritalin, their dopamine levels and their attention deficits went back to normal.
“Prior to our study, there was no molecular basis for using Ritalin to treat children with NF1 and attention deficits, so its use depended on the pediatrician’s practice, the severity of the attention deficit and how comfortable the parents were with the use of medication,” Gutmann says. “In general, only the most severely affected kids are being treated, but that may change in the future.”
For the current study, Gutmann joined forces with Robert Mach, PhD, professor of radiology, who had been working with raclopride, an imaging agent that binds to dopamine receptors in the brain. Raclopride can be detected by positron emission tomography (PET) scans.
Jinbin Xu, PhD, research instructor in radiology, used raclopride to evaluate dopamine levels in untreated mice and discovered that lower levels of brain dopamine allowed for better raclopride binding, creating a stronger PET image. After Ritalin treatment, the raclopride binding decreased.
“This finding suggested that raclopride PET imaging could be used as a platform for preclinical testing of drugs that may affect brain dopamine levels,” Gutmann says. “We can get an image in an hour and assess the effects of the drug on mouse behavior in a day.”
“At some point, we envision a prescreening process that identifies children with reduced dopamine levels most likely to respond to Ritalin or other medications,” Gutmann says. “As we learn more about the different ways attention deficits arise in these children, it may be possible to use the prescreening data and preclinical drug tests in mouse models to select the best drug for each patient.”
Consider the power of the human brain
Consider the human brain.
Despite weighing only three pounds, the human brain is the most complex structure in the body. The brain encases more than 100 billion cells and is capable of sending signals to thousands of other cells at speeds of more than 200 miles per hour.
Throughout its lifetime, the brain will establish trillions of connections within the body. All that power -- and we still manage to forget where we put our vehicle keys.
The human brain really is an incredible machine. It goes far beyond any man-made computers in terms of its complexity and capability.
Our brain serves as the command and control center of the body. This enables various organs to function while simultaneously helping us operate at an intellectual level, retaining facts, learning to reason and thinking.
The mind is one of God's most fascinating creations. But, we must guard our thoughts.
"Self-control is primarily mind-control," John Stott said.
J.J. Oswald Sanders states, "The mind of man is the battleground on which every moral and spiritual battle is fought."
The Lord Jesus gives everyone hope and help with this key truth: We are to love God with all our minds.
Despite weighing only three pounds, the human brain is the most complex structure in the body. The brain encases more than 100 billion cells and is capable of sending signals to thousands of other cells at speeds of more than 200 miles per hour.
Throughout its lifetime, the brain will establish trillions of connections within the body. All that power -- and we still manage to forget where we put our vehicle keys.
The human brain really is an incredible machine. It goes far beyond any man-made computers in terms of its complexity and capability.
Our brain serves as the command and control center of the body. This enables various organs to function while simultaneously helping us operate at an intellectual level, retaining facts, learning to reason and thinking.
The mind is one of God's most fascinating creations. But, we must guard our thoughts.
"Self-control is primarily mind-control," John Stott said.
J.J. Oswald Sanders states, "The mind of man is the battleground on which every moral and spiritual battle is fought."
The Lord Jesus gives everyone hope and help with this key truth: We are to love God with all our minds.
Neuroscientist peers into own drug-altered brain
Marc Lewis' rock 'n' roll lifestyle in 1969 included every drug he could find -- or steal.
“It was a challenge to see if I could write a book that wove an account of what’s going on in your brain in parallel with what’s going on in your life,” Lewis explained in an interview. “The thing I knew best was my own story. And the most intense roller-coaster part of my life was the addiction.”
Lewis grew up in the affluent suburb of York Mills in the 1960s, then as a young teen was sent to New England to attend private school. His spiral into drug use started after his arrival there. Leaving York Mills Collegiate and his family in Canada to go to Tabor Academy, a preparatory school in Massachusetts, was such an emotional wrench that he slumped into depression. He sought release first through alcohol, then other drugs.
He eventually enrolled for a B.A. at Berkeley — a hotbed for radical politics and drugs such as LSD. He dropped out after two years and had the luck to move to Kuala Lumpur where his father worked as a doctor. It was very easy there to get drugs. “I was infatuated with drugs,” Lewis writes. “Their scent was everywhere, in my father’s medical connections and in the half-hearted legal restrictions of the society at large. I kept my eyes and ears open. . . There was a lot to explore for an intrepid druggie.”
Lewis experimented with marijuana, dextromethorphan (found in cough syrup), LSD, methamphetamine, Demerol, Percodan, morphine, heroin, opium and every kind of whacked-out pharmaceutical he could buy or steal. Except crack. It wasn’t invented yet.
Living in Malaysia led Lewis to explore neighbouring countries, places where it was easy to get opium. “In the early seventies there was a well-known path that passed through Indonesia, Singapore, Bangkok, Vientiane (in Laos), Chiang Mai (a city in northern Thailand), and Burma, then emptied like a sewer into India, where it branched off to Calcutta, Varanasi, and Goa, or north to Darjeeling and Kathmandu (in Nepal),” he writes. “This was where the young and displaced from the U.S., Canada, Britain, Germany, France and Australia went to find adventures — the intra-psychic variety supplied by drugs and the geographic and cultural variety found in every town and village.”
Lewis contracted hepatitis several times, stole drugs from his father in Malaysia and later from university labs where he did research. “I would shoot morphine in the university library, sitting on the toilet,” he writes. “Then I would walk through the stacks, intent on the subterfuge. Devoted student or despicable addict? Who would ever know? Who could even guess?” His first marriage ended badly and he began to break into medical centres and even into homes searching through strangers’ drug cabinets, looking for his next high.
All the time his brain was changing as it was being bombarded with the chemicals he subjected himself to. He illustrates this with diagrams and easy-to-comprehend scientific description. When one takes opium, he explains, it feels good in two ways. “First, by inhibiting the firing of neurons that are activated by pain or stress. These neurons are found all over the brain, in locations such as the spinal cord where pain is first processed; the brain stem; a region of the cortex called the insula, where pain and other feelings are felt and made conscious; the amygdala, where emotional reactions are orchestrated; and even the prefrontal cortex, where the world is evaluated and acted upon.
“The second way opioids make you feel good is by targeting receptors in a very specific brain region: the ventral striatum,” he writes. This is the home of motivation, wanting, desire. “At the brain level, opioids in the ventral striatum cause the feeling of wellbeing, but then they trigger dopamine release, enhancing the appeal of whatever’s showing up on the screen of perception. Natural goodies like food and sex certainly follow the progression from liking to wanting. Feels good — want more.”
It was when he was a psychology graduate student at the University of Windsor in the late ’70s that things blew apart. He was interning at Lakehead Psychiatric Hospital where he began stealing drugs, much as he had in the past and he became hooked on methamphetamine — speed. One night, as he searched through a hospital clinic looking for drugs to steal, he was nabbed by police. Again. But this time it was serious. He was not a kid anymore and he had to hire a lawyer and risk going to jail. Luckily, he was able to get letters of commendation from professors, psychologists and friends and was sentenced to months of probation But his story made the local newspaper and he was kicked out of the University of Windsor.
After that run-in with the law, Lewis finally quit his addictions, began psychotherapy and went back to university, becoming a professor of child psychology.
He recognizes he may have altered the workings of his brain forever. “The brain changes with addiction. Not in one or two systems, but in dozens. Neuroscientists are still trying to crack the problem, and each year they find more changes: changes in dopamine flow, changes in sensitivity to dopamine, changes in other neuromodulators such as acetylcholine, changes in the striatum, the amygdala, the hippocampus, the hypothalamus, and profound changes in the prefrontal cortex, the seat of appraisal, judgment and consciousness itself.”
Mind-altering drugs fail, in the long run, to fulfill the need for relations with others, he learned: “Once addiction sets in, the brain will never return to the state — of innocence? — that preceded it.”
Lewis spent five years studying the neuroscience of how the brain is affected by drugs and writing his memoir. His life is good now, he says. He is remarried and is the father of twin girls, 5 years old. He teaches at Radboud University in the Netherlands where he moved last year after a professorship at the University of Toronto. He lives across the road from the Rhine River. He went through hell to get there, true, but somehow, unlike Orpheus who looked back into the underworld as he made his ascent, Lewis has been able — despite a recent operation on his spine which required painkillers — to resist the pull of addiction.
And write a very compelling book.
Keep your brain working
Difference between normal memory loss with ageing and something that’s concerning has to do with frequency and persistence,
Memory lapses can be aggravating, frustrating and even embarrassing. But the truth is that occasional memory blips in your 30s — and even 40s and 50s — rarely signal a serious problem, says Susan Lehmann of the Geriatric Psychiatry Clinic at Johns Hopkins Hospital.
“It’s typically more about distraction and how much information the human brain can handle at one time,” she says. “All the complexities of life make it easy, in any one day, to forget something.” In other words, if you’re distracted by a screaming child or bills or a nearby television while you’re reading a novel, you’re probably not making memories properly and thus may have difficulty recalling characters, plot twists and other details.
“The most reliable observation about memory in the course of getting older is the slowing of the identification of specific bits of information — like trying to recall a person’s name when you meet them in unexpected circumstances and there’s only three seconds where it’s socially appropriate to say, ‘Hello, Bill,’ and you just can’t get there in time,” he says.
“Older people can concentrate just as long as younger ones without distraction, but it usually takes a bit longer to process and absorb a task, and (they) also have a little bit more difficulty in switching tasks and multi-tasking,” adds Lehmann.
Those of us who do forget a phone number or an appointment here or there aren’t necessarily doomed to more serious cognitive impairment later on. “Though they make people anxious, the normal memory changes that happen as you age through midlife and beyond — which tend to be episodic, occasional and stable — are not a risk factor for Alzheimer’s disease or dementia,” says Lehmann. “The difference between normal memory loss with ageing and something that’s concerning has to do with frequency and persistence, and how much it starts to interfere with everyday life and your ability to function and work.”
Indeed, Lehmann stresses that cognitive decline isn’t an inevitable part of ageing: “There is a lot of variability among people.” A study published last month in the journal Lancet Neurology summarised evidence from hundreds of studies and found that up to half of all Alzheimer’s cases are associated with seven modifiable risk factors, including midlife obesity, depression and cognitive inactivity or low educational attainment.
While it remains unclear whether Alzheimer’s can be prevented, experts believe that most of us have at least some control over our long-term brain health. “You can’t stop ageing, you can’t change your family history or genetics, but you can make some basic lifestyle choices that may help with age-related cognitive decline and also more serious problems,” says neurologist Scott Turner, director of the Memory Disorders Programme at Georgetown University Medical Centre. He recommends an integrated wellness approach that includes a Mediterranean diet that’s high in antioxidants, regular exercise and keeping your mind engaged and challenged, whether it’s with crossword puzzles or more formal study.
“The earlier you start doing these things, the better,” says Turner. As the Lancet research points out, it’s also important to prevent or treat vascular risk factors such as high blood pressure, diabetes and smoking. “The kinds of health conditions that predispose somebody to heart attack and stroke increase risk for dementia, too,” says Lehmann.
In the interest of having as many resources at your disposal as possible, clinical psychologist Cynthia Green, author of 30 Days to Total Brain Health, offers four tips for staving off memory loss
Memory lapses can be aggravating, frustrating and even embarrassing. But the truth is that occasional memory blips in your 30s — and even 40s and 50s — rarely signal a serious problem, says Susan Lehmann of the Geriatric Psychiatry Clinic at Johns Hopkins Hospital.
“It’s typically more about distraction and how much information the human brain can handle at one time,” she says. “All the complexities of life make it easy, in any one day, to forget something.” In other words, if you’re distracted by a screaming child or bills or a nearby television while you’re reading a novel, you’re probably not making memories properly and thus may have difficulty recalling characters, plot twists and other details.
“The most reliable observation about memory in the course of getting older is the slowing of the identification of specific bits of information — like trying to recall a person’s name when you meet them in unexpected circumstances and there’s only three seconds where it’s socially appropriate to say, ‘Hello, Bill,’ and you just can’t get there in time,” he says.
“Older people can concentrate just as long as younger ones without distraction, but it usually takes a bit longer to process and absorb a task, and (they) also have a little bit more difficulty in switching tasks and multi-tasking,” adds Lehmann.
Those of us who do forget a phone number or an appointment here or there aren’t necessarily doomed to more serious cognitive impairment later on. “Though they make people anxious, the normal memory changes that happen as you age through midlife and beyond — which tend to be episodic, occasional and stable — are not a risk factor for Alzheimer’s disease or dementia,” says Lehmann. “The difference between normal memory loss with ageing and something that’s concerning has to do with frequency and persistence, and how much it starts to interfere with everyday life and your ability to function and work.”
Indeed, Lehmann stresses that cognitive decline isn’t an inevitable part of ageing: “There is a lot of variability among people.” A study published last month in the journal Lancet Neurology summarised evidence from hundreds of studies and found that up to half of all Alzheimer’s cases are associated with seven modifiable risk factors, including midlife obesity, depression and cognitive inactivity or low educational attainment.
While it remains unclear whether Alzheimer’s can be prevented, experts believe that most of us have at least some control over our long-term brain health. “You can’t stop ageing, you can’t change your family history or genetics, but you can make some basic lifestyle choices that may help with age-related cognitive decline and also more serious problems,” says neurologist Scott Turner, director of the Memory Disorders Programme at Georgetown University Medical Centre. He recommends an integrated wellness approach that includes a Mediterranean diet that’s high in antioxidants, regular exercise and keeping your mind engaged and challenged, whether it’s with crossword puzzles or more formal study.
“The earlier you start doing these things, the better,” says Turner. As the Lancet research points out, it’s also important to prevent or treat vascular risk factors such as high blood pressure, diabetes and smoking. “The kinds of health conditions that predispose somebody to heart attack and stroke increase risk for dementia, too,” says Lehmann.
In the interest of having as many resources at your disposal as possible, clinical psychologist Cynthia Green, author of 30 Days to Total Brain Health, offers four tips for staving off memory loss
Wright educates public on concussions
FILE - This Sept. 2011 file photo
shows Patriots' Mike Wright on the sideline during the fourth quarter of a
preseason game against the Giants at Gillette Stadium in Foxboro, Mass.
Wright's season ended prematurely due to a concussion for the second
straight year on Thursday when the Patriots placed the veteran defensive
lineman on injured reserve.
Wright’s emotional message on Friday even traveled right down to the high school and mighty mite level.
Wright, who was placed on season-ending IR (injured reserve list) for his second concussion in less than two years, somberly spoke to the media about the importance of the brain bruise he sustained in the season opener against the Miami Dolphins.
"I was thinking about coming back in the next couple weeks," Wright said. "But based on my concussion history...coaches, doctors and trainers are looking out for my best interest and my health. I did not want to go on the IR. It was the last thing I wanted to do. I was looking forward to being a part of this team. It was just the right decision."
Wright first sustained a concussion in last season’s game against the Colts on Nov. 21 when he collided with then teammate Tully Banta-Cain, who made significant contact with Wright’s helmet.
Throughout his ordeal after the concussion, Wright said it challenging for him. He experienced trouble watching television, being on the computer and reading books.
This year, Wright was excited in training camp and made it back to the field against the Dolphins. But the hopes of a new season quickly evaporated after taking another blow to the head.
"In college, you don’t think about these injuries," Wright said. "It’s not a big deal, having your head a little sore. I have a new found respect for the brain and what it does just based on what I’ve dealt with."
Concussions are now the talk of all sports from elementary school to the professional level.
Dr. Ricardo Komotar, Director of Surgical Neuro-Oncology and neurosurgeon at the University of Miami Hospital spoke about the dangers and signs athletes must understand when sustaining even a minor concussion.
"Most concussions have a loss of consciousness," Komotar said. "But a player doesn’t have to be knocked out cold in order to have a concussion. Athletes develop a loss of short-term memory, severe headache and difficulty concentrating. The person knows something is off.
"When you’re dealing with multiple concussions, you’re putting your long-term mental health at risk, not just short-term. The chance of getting back to 100 percent normal becomes less. My strategy after the third concussion is a wrap. Now the chance of long-term chronic, permanent brain damage is higher. In my perspective, three is the cutoff."
Komotar spoke about former Bengal receiver Chris Henry, who in 2009 died when he fell out of a moving truck in Charlotte N.C.
A year later, the Brain Injury Research Institute of West Virginia released a report stating Henry developed a brain disease called chronic traumatic encephalopathy during his playing career due to multiple hits to the head.
"You look at the type of athlete playing in the sport," Komotar said. "People are bigger, stronger and faster. I think just the evolution of the athlete... the speed, the velocity, the mass and energy on contact. Just the overall size of the athlete. Our recognition of the injury has gone up so much. I think now the general education of physicians, players and the public in general are so much higher."
Wright said concussions are no joke.
"I have a long life to live and a lot of things to look forward to," Wright said. "You have to put things in perspective. You just take a lot of things for granted. You love the game. It’s a process and routine that you get a custom through the years.
"Football is a game of toughness...there’s a lot of things you do push through but there are things that you have to paid attention to that can affect you in a serious way. You can’t even imagine."
Wright has this message for high school football players.
"This game is awesome and I think the best in the world," he said. "Being a tougher sports makes it so special but you have to draw the line somewhere. Kids just need to learn from us to respect their bodies.... don’t be afraid or don’t think you’re not tough to tell somebody about what’s going on. You just have to be in tune with this. You have to respect it. The long term affects are just not worth it."
Wright hopes to convey that message to his teammates each week.
"I’ll be there in the locker room," Wright said. "Hopefully they’ll learn from my situation and helped them to move forward. Also be able to protect themselves."
Wright, 29, is a seven-year veteran who compiled 134 tackles and 15 sacks in 81 games with the Patriots. The 6-foot-4, 295-pound defensive end had been sidelined since collecting a tackle and half-a-sack in New England’s 38-24 win at Miami.
Wright, who was teary eyes throughout, concluded the press conference with this.
"Your brain is extremely important," Wright said. "You don’t even know what your brain has to process to get out of a chair. I think its great what the NFL is trying to do to educate everyone...I think the kids in high school level can learn a lot. When it comes to your brains...it’s very, very serious....its nothing to play with....not only in the NFL but college and high school. Kids can educate themselves and get a little bit hold of these injuries."
Bilingual babies help experts learn how language shapes the brain
Once, experts feared that young children exposed to more than one language would suffer “language confusion,” which might delay their speech development. Today, parents are urged to capitalize on that early knack for acquiring language.
Researchers have found ways to analyze infant behavior — where babies turn their gazes, how long they pay attention — to help figure out infant perceptions of sounds and words and languages, of what is familiar and what is unfamiliar to them.
Analyzing the neurologic activity of babies’ brains as they hear language, and comparing those responses with the words the children learn as they get older, is helping explain not just how the early brain listens to language, but how listening shapes the early brain.
Differing trajectories
Recently, researchers at the University of Washington used measures of electrical brain responses to compare infants from homes in which one language was spoken to bilingual infants. Of course, since the subjects of the study ranged from 6 months to 12 months of age, they weren’t producing many words in any language.
Still, the researchers found that at 6 months, the monolingual infants could discriminate between phonetic sounds, whether they were uttered in the language they were used to hearing or in another language not spoken in their homes. By 10 to 12 months, however, monolingual babies were no longer detecting sounds in the second language, only in the language they usually heard.
The researchers suggested that this represents a process of “neural commitment,” in which the brain wires itself to understand one language and its sounds.
The bilingual infants followed a different developmental trajectory. At 6 to 9 months, they did not detect differences in phonetic sounds in either language, but at 10 to 12 months, they were able to discriminate sounds in both.
“What the study demonstrates is that the variability in bilingual babies’ experience keeps them open,” said Dr. Patricia Kuhl, co-director of the Institute for Learning and Brain Sciences at the University of Washington and one of the authors of the study. “They do not show the perceptual narrowing as soon as monolingual babies do. It’s another piece of evidence that what you experience shapes the brain.”
Learning new skills
The learning of language — and its effects on the brain — may begin even earlier than 6 months of age.
Janet Werker, a professor of psychology at the University of British Columbia, said that even in the womb, babies are exposed to the rhythms and sounds of language, and newborns have been shown to prefer languages rhythmically similar to the one they’ve heard during fetal development.
In one study, Werker and her collaborators showed that babies born to bilingual mothers not only prefer both of those languages over others — but are also able to register that the two languages are different.
And over the past decade, Ellen Bialystok, a professor at York University in Toronto, has shown that bilingual children develop crucial skills such as learning different ways to solve logic problems or handle multitasking. These skills are often considered part of the brain’s “executive function,” higher-level cognitive abilities that are localized in the frontal and prefrontal cortex.
Salk Gets $4.5M Grant for Brain Research Center
The Salk Institute for Biological Studies in La Jolla will receive a
5-year grant totaling $4.5 million from the National Institutes of
Health to establish a new research center focused on finding ways to
treat congenital brain defects and neurological diseases such as
Alzheimer’s, autism and schizophrenia.
The center will “speed discovery of how genetic changes alter abilities such as motor function, learning and memory,” said Salk Institute President William R. Brody.
The new Neuroscience Core Center is one of three brain research centers established nationally this year by the National Institute of Neurological Disorders and Stroke, which is a unit of Bethesda, Md.-based NIH. The center will be led by Dennis O'Leary, the Vincent J. Coates Professor of Molecular Neurobiology at Salk, and it will provide research support in three areas that are particularly important for neuroscience: genome manipulation, imaging and behavioral studies, according to an Oct. 13 Salk statement.
O’Leary said that brain researchers are increasingly focused on the links between genes and behavior, exploring how genetics play a role in brain development, “which is ultimately manifested in a person's ability to function.”
More than half of Salk's 58-person faculty is engaged in neuroscience research. “The center will provide Salk scientists access to new research technologies and free them from having to reinvent the wheel for each new project,” O’Leary said. “This center will be an exponential boost to our ability to do cutting-edge research in neuroscience.”
The center will “speed discovery of how genetic changes alter abilities such as motor function, learning and memory,” said Salk Institute President William R. Brody.
The new Neuroscience Core Center is one of three brain research centers established nationally this year by the National Institute of Neurological Disorders and Stroke, which is a unit of Bethesda, Md.-based NIH. The center will be led by Dennis O'Leary, the Vincent J. Coates Professor of Molecular Neurobiology at Salk, and it will provide research support in three areas that are particularly important for neuroscience: genome manipulation, imaging and behavioral studies, according to an Oct. 13 Salk statement.
O’Leary said that brain researchers are increasingly focused on the links between genes and behavior, exploring how genetics play a role in brain development, “which is ultimately manifested in a person's ability to function.”
More than half of Salk's 58-person faculty is engaged in neuroscience research. “The center will provide Salk scientists access to new research technologies and free them from having to reinvent the wheel for each new project,” O’Leary said. “This center will be an exponential boost to our ability to do cutting-edge research in neuroscience.”
Brain scans show being bilingual can delay Alzheimer's
Tom Schweizer, a neuroscientist at St. Michael's Hospital appears on Canada AM, Friday, Oct. 14, 2011.
You may have heard it before: being bilingual can help ward off
dementia. Now, a new study offers the brain scans to back up those
findings.
A number of studies in recent years have shown that knowing more than one language and speaking them regularly can delay the onset of dementia. Those studies reached their conclusions by looking at bilingual and monolingual seniors and then noting the age at which the patients began to decline cognitively with memory problems, attention problems and difficulty with planning and organization.
This new study from Toronto researchers included CT (computed tomography) brain scans of patients who had been diagnosed with probable Alzheimer's disease and who had similar levels of education and cognitive skills.
The team found that the scans of the bilingual patients showed twice as much damage in areas of the brain known to be affected by Alzheimer's. And yet, cognitively, these patients were doing as well as their monolingual counterparts.
The finding suggests that being bilingual somehow preserves cognitive function, even with areas of the brain being destroyed by disease, says Dr. Tom Schweizer, a neuroscientist at St. Michael's Hospital who led the study.
"What we noticed was that in the areas associated with Alzheimer's pathology -- so that's the temporal cortex, which is the area of the brain that serves memory function -- we noticed that the bilingual patients had twice as much atrophy in those areas than the monolingual patients," Schweizer explained to CTV's Canada AM.
"That's interesting because, despite the extra disease burden in the bilingual patients, they maintained their level of cognitive performance as well as monolingual patients."
The study, which appears in the journal Cortex, was small, involving just 40 patients, half of whom were fluent in another language. But it's being called the first to provide physical evidence to confirm the previous research on the topic.
While it should stand to reason that brains that look more damaged would perform worse on thinking tests, Schweizer theorizes that being bilingual somehow protects the brain, boosting its "cognitive reserve" and resilience to damage.
It's still unclear how being bilingual protects the brain. Schweizer says it could be that bilingual people who are constantly switching from one language to another are exercising their brain without even realizing it.
"We think it's enhancing neural networks in the brain; it's actually making the brain a little more efficient and so it can probably compensate for any type of disease process," he explained.
The study authors say that while being bilingual might delay the onset of dementia symptoms, bilingualism can't prevent dementia.
But they say more study is needed to determine whether, once dementia symptoms appear, the disease progresses faster in bilingual people than monolingual patients.
They'd also like to know whether a second language has to be learned early in life to provide the most benefit.
The team would like to repeat the study in a larger sample of patients, using more sophisticated MRIs, which do a better job of noting brain damage.
The concept that one can build up "cognitive reserve" is one of the reason that why many physicians encourage older people to do brain work, like crossword or Sudoku puzzles, says Schweizer.
"You may not want to pick up another language; you may want to learn a musical instrument -- anything to exercise the brain and keep it active in your retirement years, and hopefully before that so you can keep that ball rolling."
A number of studies in recent years have shown that knowing more than one language and speaking them regularly can delay the onset of dementia. Those studies reached their conclusions by looking at bilingual and monolingual seniors and then noting the age at which the patients began to decline cognitively with memory problems, attention problems and difficulty with planning and organization.
This new study from Toronto researchers included CT (computed tomography) brain scans of patients who had been diagnosed with probable Alzheimer's disease and who had similar levels of education and cognitive skills.
The team found that the scans of the bilingual patients showed twice as much damage in areas of the brain known to be affected by Alzheimer's. And yet, cognitively, these patients were doing as well as their monolingual counterparts.
The finding suggests that being bilingual somehow preserves cognitive function, even with areas of the brain being destroyed by disease, says Dr. Tom Schweizer, a neuroscientist at St. Michael's Hospital who led the study.
"What we noticed was that in the areas associated with Alzheimer's pathology -- so that's the temporal cortex, which is the area of the brain that serves memory function -- we noticed that the bilingual patients had twice as much atrophy in those areas than the monolingual patients," Schweizer explained to CTV's Canada AM.
"That's interesting because, despite the extra disease burden in the bilingual patients, they maintained their level of cognitive performance as well as monolingual patients."
The study, which appears in the journal Cortex, was small, involving just 40 patients, half of whom were fluent in another language. But it's being called the first to provide physical evidence to confirm the previous research on the topic.
While it should stand to reason that brains that look more damaged would perform worse on thinking tests, Schweizer theorizes that being bilingual somehow protects the brain, boosting its "cognitive reserve" and resilience to damage.
It's still unclear how being bilingual protects the brain. Schweizer says it could be that bilingual people who are constantly switching from one language to another are exercising their brain without even realizing it.
"We think it's enhancing neural networks in the brain; it's actually making the brain a little more efficient and so it can probably compensate for any type of disease process," he explained.
The study authors say that while being bilingual might delay the onset of dementia symptoms, bilingualism can't prevent dementia.
But they say more study is needed to determine whether, once dementia symptoms appear, the disease progresses faster in bilingual people than monolingual patients.
They'd also like to know whether a second language has to be learned early in life to provide the most benefit.
The team would like to repeat the study in a larger sample of patients, using more sophisticated MRIs, which do a better job of noting brain damage.
The concept that one can build up "cognitive reserve" is one of the reason that why many physicians encourage older people to do brain work, like crossword or Sudoku puzzles, says Schweizer.
"You may not want to pick up another language; you may want to learn a musical instrument -- anything to exercise the brain and keep it active in your retirement years, and hopefully before that so you can keep that ball rolling."
Video games 'can alter children's brains'
The average child will spend almost 2,000 hours in front of a screen between their tenth and eleventh birthdays
Children should "feel the grass under their feet" rather than play
addictive computer games which can harm their mental development, a leading
scientist has said.
Children should "feel the grass under their feet" rather than play
addictive computer games which can harm their mental development, a leading
scientist has said.
Baroness Greenfield, the former director of the Royal Institution, said
spending too much time staring at computer screens can cause physical
changes in the brain that lead to attention and behaviour problems.
Technology that plays strongly on the senses – like video games – can
literally "blow the mind" by temporarily or permanently
deactivating certain nerve connections in the brain, the Baroness said.
She told the Daily Telegraph last night: "The human brain has evolved to
adapt to the environment. It therefore follows that if the environment is
changing, it will have an impact on your brain.
"If you play computer games to the exclusion of other things this will
create a new environment that will have new effects ... every hour you spend
in front of a screen is an hour not spent climbing a tree or giving someone
a hug."
Giving a speech earlier yesterday about the addictiveness of screen
technologies at the opening of a new £2.5 million science centre at the
private Sherbourne Girls' school in Dorset, the Baroness urged pupils “to be
outside, to climb trees and feel the grass under your feet and the sun on
your face".
"Screen technologies cause high arousal, which in turn activates the
brain system’s underlying addiction and reward, resulting in the attraction
of yet more screen-based activity, the Baroness said.
The average child will spend almost 2,000 hours in front of a screen between their tenth and eleventh birthdays, she added.
Comparing the dangers to the lack of awareness about the health risks of smoking in the 1950s, she said playing too many computer games could cause a shorter attention span and more reckless behaviour in children.
Several scientific studies have suggested that playing an excessive number of computer games or spending too much time surfing the internet can have a physical impact on the brain.
A paper published earlier the summer in the PLoS ONE journal indicated that internet addiction could rewire brain structures in the inner brain, and even cause shrinkage in grey matter.
Another study by Japanese scientists ten years ago warned that because video games only stimulate the brain regions responsible for vision and movement, other parts of the mind responsible for behaviour, emotion and learning could become underdeveloped.
But other scientists have claimed that certain games can help the brain in a variety of ways such as treating post-traumatic stress disorder, boosting intelligence and developing the memory.
Jenny Dwyer, Sherborne Girls’ Headmistress, said: "Some of Baroness Greenfield’s views are controversial, which is a great thing for future classroom discussions.
"We know that her thoughts on how modern technology is changing the way we think and feel are going to provoke some lively debate among the staff and girls."
The average child will spend almost 2,000 hours in front of a screen between their tenth and eleventh birthdays, she added.
Comparing the dangers to the lack of awareness about the health risks of smoking in the 1950s, she said playing too many computer games could cause a shorter attention span and more reckless behaviour in children.
Several scientific studies have suggested that playing an excessive number of computer games or spending too much time surfing the internet can have a physical impact on the brain.
A paper published earlier the summer in the PLoS ONE journal indicated that internet addiction could rewire brain structures in the inner brain, and even cause shrinkage in grey matter.
Another study by Japanese scientists ten years ago warned that because video games only stimulate the brain regions responsible for vision and movement, other parts of the mind responsible for behaviour, emotion and learning could become underdeveloped.
But other scientists have claimed that certain games can help the brain in a variety of ways such as treating post-traumatic stress disorder, boosting intelligence and developing the memory.
Jenny Dwyer, Sherborne Girls’ Headmistress, said: "Some of Baroness Greenfield’s views are controversial, which is a great thing for future classroom discussions.
"We know that her thoughts on how modern technology is changing the way we think and feel are going to provoke some lively debate among the staff and girls."
Tuesday, October 11, 2011
Significant Reduced Loss of Brain Volume in Multiple Sclerosis Patients Treated with COPAXONE(R)
Five-year Study Findings Published in the Journal of the Neurological Sciences
JERUSALEM, Israel, Oct 11, 2011 (BUSINESS WIRE) --
Results from a five-year study of treatment-naive patients with
relapsing-remitting multiple sclerosis (RRMS) demonstrated that patients
treated with COPAXONE(R) (glatiramer acetate injection) showed
significant reduced loss of brain volume compared to patients treated
with other disease modifying therapies (DMTs).
Though all DMT treatment arms resulted in a reduction in brain volume
loss compared to the control group of non-treated patients, COPAXONE(R)
had a significantly better effect than both low and high dose
interferons, in reducing loss of brain volume. A paper published by Dr.
Omar Khan, detailing the study findings, "Effect of disease-modifying
therapies on brain volume in relapsing--remitting multiple sclerosis:
Results of a five-year brain MRI study," was recently published in the Journal
of the Neurological Sciences.
"These data represent the importance of ongoing research in a practical
clinical setting to better understand multiple sclerosis and the impact
of therapy on the course of the disease ," said Jon Congleton, Senior
Vice President and General Manager, Teva Neuroscience. "Not only does
this study highlight the benefit of COPAXONE(R) in reducing
brain volume loss, it underscores the value of early treatment in
influencing long-term outcomes."
Brain volume loss in multiple sclerosis patients exceeds the rate of
healthy control groups. Brain volume loss, sometimes referred to as
atrophy, may be correlated with cognitive and physical deficits. Modern
magnetic resonance (MR) techniques can reliably measure loss of brain
volume over time.
ABOUT THE STUDY
In the study, the COPAXONE(R) treatment arm resulted in a -2.27
percent change in brain volume (PCVB) as compared to baseline versus
-2.62 percent for Avonex(R) (low-dose interferon), -3.21
percent for Betaseron(R)/Rebif(R) (high-dose
interferon).
This was a retrospective study in which the brain magnetic resonance
imaging (MRI) scans of 275 RRMS patients treated with DMTs were examined
with Structural Image Evaluation, using Normalization of Atrophy
(SIENA). Data analysis was conducted in 2007-08 and the study period
included patients who started DMTs in 2001-02 and subsequently received
the same DMT for five years. Inclusion criteria for the study were
diagnosis of clinically definite RRMS, disease duration of five years or
less at the time of initiating DMT and treatment-naive prior to
initiation of DMT at onset of study observation period. Untreated RRMS
patients with follow-up ranging from eight to 24 months were enrolled as
controls. All untreated patients also had prior brain MRI scans on no
therapy that could be analyzed with SIENA, so that their rate of brain
volume loss was annualized and then projected over five years assuming a
constant rate of brain volume loss over five years.
121 patients in the study were treated with COPAXONE(R), 101
were treated with Betaseron(R) or Rebif(R) and 53 were
treated with Avonex(R). All patients had brain MRI scans (at
onset of DMT and five years later) on the same 1.5T scanner. Image
analysis was performed blinded to treatment allocation.
The study was supported by Wayne State University Neuroscience Program.
Preliminary results from this study were presented at the American
Academy of Neurology annual meeting in 2008.
ABOUT COPAXONE(R)
COPAXONE(R) is indicated for the reduction of the frequency of
relapses in relapsing-remitting multiple sclerosis, including patients
who have experienced a first clinical episode and have MRI features
consistent with multiple sclerosis. The most common side effects of
COPAXONE(R) are redness, pain, swelling, itching, or a lump at
the site of injection, flushing, rash, shortness of breath, and chest
pain. COPAXONE(R) (glatiramer acetate injection) is now
approved in more than 50 countries worldwide, including the United
States, Russia, Canada, Mexico, Australia, Israel, and all European
countries. In North America,
COPAXONE(R) is marketed by Teva Neuroscience, Inc., which is a
subsidiary of Teva Pharmaceutical Industries Ltd. In Europe, COPAXONE(R)
is marketed by Teva Pharmaceutical Industries Ltd. and sanofi-aventis.
COPAXONE(R) is a registered trademark of Teva Pharmaceutical
Industries Ltd.
See additional important information at:
http://www.sharedsolutions.com/pdfs/PrescribingInformation.aspx
or call 1-800-887-8100 for electronic releases.
ABOUT TEVA
Teva Pharmaceutical Industries Ltd.
/quotes/zigman/64731/quotes/nls/teva TEVA
+0.58%
is a leading global
pharmaceutical company, committed to increasing access to high-quality
healthcare by developing, producing and marketing affordable generic
drugs as well as innovative and specialty pharmaceuticals and active
pharmaceutical ingredients. Headquartered in Israel, Teva is the world's
largest generic drug maker, with a global product portfolio of more than
1,300 molecules and a direct presence in about 60 countries. Teva's
branded businesses focus on neurological, respiratory and women's health
therapeutic areas as well as biologics. Teva currently employs
approximately 42,000 people around the world and reached $16.1 billion
in net sales in 2010.
Teva's Safe Harbor Statement under the U. S. Private Securities
Litigation Reform Act of 1995:
This release contains forward-looking statements, which express the
current beliefs and expectations of management. Such statements are
based on management's current beliefs and expectations and involve a
number of known and unknown risks and uncertainties that could cause our
future results, performance or achievements to differ significantly from
the results, performance or achievements expressed or implied by such
forward-looking statements. Important factors that could cause or
contribute to such differences include risks relating to: our ability to
successfully develop and commercialize additional pharmaceutical
products, the introduction of competing generic equivalents, the extent
to which we may obtain U.S. market exclusivity for certain of our new
generic products and regulatory changes that may prevent us from
utilizing exclusivity periods, potential liability for sales of generic
products prior to a final resolution of outstanding patent litigation,
including that relating to the generic version of Protonix(R), the extent
to which any manufacturing or quality control problems damage our
reputation for high quality production, the effects of competition on
sales of our innovative products, especially Copaxone(R) (including
potential generic and oral competition for Copaxone(R)), the impact of
continuing consolidation of our distributors and customers, our ability
to identify, consummate and successfully integrate acquisitions
(including the acquisition of Cephalon), interruptions in our supply
chain or problems with our information technology systems that adversely
affect our complex manufacturing processes, intense competition in our
specialty pharmaceutical businesses, any failures to comply with the
complex Medicare and Medicaid reporting and payment obligations, our
exposure to currency fluctuations and restrictions as well as credit
risks, the effects of reforms in healthcare regulation, adverse effects
of political or economical instability, major hostilities or acts of
terrorism on our significant worldwide operations, increased government
scrutiny in both the U.S. and Europe of our agreements with brand
companies, dependence on the effectiveness of our patents and other
protections for innovative products, our ability to achieve expected
results through our innovative R&D efforts, the difficulty of predicting
U.S. Food and Drug Administration, European Medicines Agency and other
regulatory authority approvals, uncertainties surrounding the
legislative and regulatory pathway for the registration and approval of
biotechnology-based products, potentially significant impairments of
intangible assets and goodwill, potential increases in tax liabilities
resulting from challenges to our intercompany arrangements, our
potential exposure to product liability claims to the extent not covered
by insurance, the termination or expiration of governmental programs or
tax benefits, current economic conditions, any failure to retain key
personnel or to attract additional executive and managerial talent,
environmental risks and other factors that are discussed in our Annual
Report on Form 20-F and other filings with the U.S. Securities and
Exchange Commission.
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