Tuesday, March 9, 2010

Great Minds

Having a greater sense of purpose in life may help fend off Alzheimer’s disease as we age.
People who feel good about what they have done in their lives and look forward to what they will accomplish in the future feel a greater sense of purpose in life, making them less likely to suffer cognitive decline and its possible consequence, Alzheimer’s disease. While researchers say that there is no specific biological basis named for this connection, it may be connected to stronger immune function and blood vessel health, the study team, led by Patricia A. Boyle, PhD, of Rush University Medical Center in Chicago, says. 

A sense of purpose is defined in the study as a "psychological tendency to derive meaning from life's experiences and to possess a sense of intentionality and goal directedness that guides behavior."

Dr. Sandi Chapman, executive director at the Center for BrainHealth, says that our attitudes can affect our brain health.“Research shows that people who are optimistic develop more robust brain function and stronger brain connections; therefore, they stay mentally viable longer,” Chapman, who was not involved in the study, explains. “Those who develop a strong purpose in life have stronger mental function as well.”  
The research is important in that it examines the notion of finding purpose in one’s life beyond the limits of what has been previously studied, says Cynthia Green, PhD, assistant clinical professor in the Department of Psychiatry at Mount Sinai School of Medicine.
Green, who was not involved in the study, says that the results, particularly those stating that a reduced risk of dementia is connected with a sense of purpose, are “fascinating.”
“What distinguishes successful agers [from their peers] is a sense of resilience—emotional resilience," Green explains. “There is a qualitative aspect of well-being that we don’t always measure when we look at cognitive impairment.”   
We have more control than we realize over our cognitive health, she adds. “There is a lot that we can do in terms of how we function and the choices we make and how we see ourselves that impact our long term health and well being,” Green, whose latest book, Brainpower Game Plan  focuses on ways to sharpen memory, concentration, and “age-proofing” your mind, maintains.
While eating a nutritious diet, maintaining a healthy weight, and staying physically active have all been touted as factors, emotional health and “the spirit side of brain health,” she notes, have not been as openly recognized because “those are hard to measure from a quantifiable perspective.”
“What is unique about this study is that is about one’s own personal sense of purpose. This is a step beyond, more abstract and removed,” Green explains. “Thinking of one’s own legacy, Boomers can reflect on one’s sense of purpose, what you want to leave as your mark, pursuing that provides opportunities for continued engagement, and being intellectually and socially engaged.”

Still, there are some mysteries of nature that are difficult to solve, Chapman concludes. “It is still a bit of the chicken-and-egg scenario, as there are many older folks who tend to be crotchety or mean—and never develop any type of Alzheimer’s or dementia.”

Ark Pulls MAA Covering Gene-Based Therapy for Brain Cancer

Ark Therapeutics has withdrawn the MAA for its lead gene-based treatment for operable malignant glioma, Cerepro®. The move follows a request by the EMEA’s Scientific Advisory Group on Oncology (SAG-O) for an additional clinical trial with the treatment.
Ark says that it is now reviewing its portfolio of assets and has initiated discussions with a number of parties that might lead to a takeover bid. The firm stressed that an offer is by no means a certainty, and it is considering alternative strategies and options to optimize shareholder value.
The SAG-O’s re-evaluation of the Cerepro marketing application concluded that existing trial data did not provide sufficiently reliable evidence of a clinical benefit. In particular, concerns related to the lack of standardized decision-making with respect to re-intervention following tumor recurrence. This meant that data on the primary endpoint could not be considered reliable, despite the use of a blinded re-intervention committee and the Phase III data showing no evidence of bias on all available re-intervention related study measurements, the company notes.
“We are naturally disappointed with this news,” comments Nigel Parker, Ark’s CEO. “Whilst there are differences of opnion  concerning the data relating to the re-intervention endpoint, we are in a unique position, with all the barriers in relation to approval of the gene medicine components of Cerepro behind us, and the recommendation for a further trial to resolve outstanding concerns is the logical way forward to secure marketing approval.”
The MAA application for Cerepro was filed in November 2008 and underwent formal review via the centralized procedure. The European Committee for Medicinal Products for Human Use (CHMP) adopted a negative opinion on the MAA in December 2009. In February Ark filed documentation with the EMEA relating to its request for re-examination of the MAA.
In January Ark confirmed it was reprioritizing its product development programs and would cut jobs to preserve cash. Pipeline reprioritization included the decision to put further Phase III development of its cancer cachexia drug candidate, Vitor™, on hold, while continuing with Phase III development of Trinam®, a gene-based therapy to prevent blood-vessel blocking in kidney dialysis patients who have undergone vascular access graft surgery.
The firm also aimed to push on with taking its key preclinical programs into Phase I/IIa development. These include EG011 in refractory angina, EG016 in peripheral vascular disease, and EG013 in fetal growth retardation.

McGovern Institute to acquire new brain imaging technology

Magnetoencephalography (MEG) is a powerful and noninvasive method for studying human brain activity.
Elekta, Inc.

MEG works by detecting the tiny (femtotesla) magnetic fluctuations at the surface of the head that arise from the brain’s electrical activity. Unlike MRI, MEG can measure the timing of brain activity with millisecond precision, allowing researchers to study the rapid brain events that underlie human cognition. 

The new MEG scanner will operate as a shared core facility for the local neuroscience community, and will be used for a wide range of studies, including basic research on human cognition in adults and children as well as studies of autism, dyslexia, depression, schizophrenia and other disorders. There will also be an emphasis on technology development — progress in MEG depends on advances in signal processing, and Gabrieli hopes to engage MIT’s expertise in computer science and engineering to push the capabilities of MEG technology.

MEG was developed at MIT in 1969 by David Cohen, who exploited the newly invented SQUID detectors that provided the necessary sensitivity to measure the brain’s tiny magnetic signals. The new MIT scanner, an Elekta Neuromag, will have an array of 306 such detectors, providing a detailed spatial view of the signal sources far beyond what was possible 40 years ago. It will be housed in a magnetically shielded room to protect the sensitive detectors from background noise.  

The purchase of a new MEG system has been made possible by grants from the National Science Foundation and the Simons Foundation, and by philanthropic support to the McGovern Institute from Thomas F. Peterson ‘57, Edward and Kay Poitras, and an anonymous donor. Construction will begin this month, and the scanner is expected to be operational by fall. 

Anyone interested in learning more should contact Charles Jennings, director of the McGovern Institute Neurotechnology (MINT) program at charlesj@mit.edu.

Ritalin Boosts Brain Plasticity And thus promotes learning

In a new study conducted on animals, researchers discovered that the common medication Ritalin actually had the potential to improve focus and also to promote the ability to learn. The drug works on synapses, promoting the release of the neurotransmitter dopamine, which plays an important role in allowing neurons to communicate with each other, and therefore in promoting focus. In the research, Ritalin proved capable of boosting brain plasticity as well, as in the strength of synapses, the connections between neurons, e! Science News reports.

“Since we now know that Ritalin improves behavior through two specific types of neurotransmitter receptors, the finding could help in the development of better targeted drugs, with fewer side effects, to increase focus and learning,” says University of California in San Francisco (UCSF) professor of neurology Antonello Bonci, MD. He was also the principal investigator of the new paper, and a member of the UCSF Department of Neurology Ernest Gallo Clinic and Research Center. The new work was only made possible by previous studies, which demonstrated that neural plasticity is a trait that continues throughout life, and does not stop once a person reaches adulthood.

“We found that a dopamine receptor, known as the D2 receptor, controls the ability to stay focused on a task – the well-known benefit of Ritalin. But we also discovered that another dopamine receptor, D1, underlies learning efficiency,” says UCSF expert Patricia Janak, PhD. She, alongside Bonci, is a co-senior author of a new paper detailing the findings, which appears in the March 7 online issue of the respected scientific publication Nature Neuroscience. The team was able to determine that one of the primary therapeutic targets of Ritalin is the almond-shaped cluster of neurons called the amygdala, which is known to play a crucial role regulating learning, emotional memory and fear.

“Although Ritalin is so frequently prescribed, it induces many brain changes, making it difficult to identify which of those changes improve learning. By identifying the brain mechanisms underlying Ritalin's behavioral enhancements, we can better understand the action of Ritalin as well as the properties governing brain plasticity,” says former Gallo Center postdoctoral scientist Kay M. Tye, PhD. In the new experiments, the animals being tested were given Ritalin doses equivalent to the ones children regularly take. Therefore, the team says, there may be a high chance of the findings remaining valid for humans as well.

Study: Nicotine Takes Time To Accumulate In Brain

A new study shows that nicotine builds up in the brain over the course of smoking a whole cigarette.

   Researchers at Duke University Medical Center put to rest the idea that each puff on a cigarette causes a spike of nicotine to the brain.

   In fact, it takes a while for the nicotine to reach its peak effect.

   The researchers used a PET scan on 13 addicted smokers and ten non-addicted smokers to see which parts of the brain lit up and when.

   The addicts took longer to get all the nicotine up to their brains, which surprised researchers.

   Researchers theorize that it's because the nicotine lingers longer in their damaged lungs.

   The bottom line was that both the addicted and non-addicted smokers ended up with similar amounts of the stimulant in their brains.

   The Duke researchers don't have any good answers why some people are more prone to being addicted to smoking than others.

   The study is published in the journal "Proceedings of the National Academy of Sciences."

Dealing with Alzheimers


What is Alzheimer’s disease? Many people are unaware of the symptoms and pain it could cause someone very close to you. In this article one will find valuable information about how you can look out for signs and symptoms of Alzheimer’s and how you can care for someone with it.

Alois Alzheimer discovered the disease in 1906. Over the years scientists have described Alzheimer’s as a progressive and fatal brain disease. It is a disease that destroys brain cells that cause memory loss and can cause problems with thinking and behavior that can affect activities in everyday life. It is a disease that only gets worse over time and there is no cure, however there are medications that are known to slow down the process.

Over 5.3 Americans suffer from Alzheimer’s and it is the seventh leading cause of death in the United States. What is the cause? Scientists aren’t exactly sure how a patient develops Alzheimer’s but it has been said that it can be obtained through genetics or different environmental factors.

Symptoms of Alzheimer’s vary from person to person but the most common side effects are, memory loss, forgetting things like names of people, and even relationships one has with another individual. As the disease progresses symptoms may worsen. Someone with the disease could forget how to get somewhere they have been a dozen times and also they may start to feel nervous or sad at times. Some people will drive somewhere and completely forget how they got there.

People with Alzheimer’s eventually need someone by their side almost 24 hours a day once the disease gets to a critical point.

“Caring for someone with Alzheimer’s can be very challenging at times, you know they need someone to help them at all times so you must be very patient with them, or else it could make their condition worse,” Cindy Duga, RN at DePaul hospital said.

Everyone with Alzheimer’s deals with it differently than others. There are many ways to care for someone with this disease. Here are a few ways you can be of help to a diagnosed individual. Make sure they are doing enough daily activities, having things to do in their day sometimes helps relieve the feeling of being lost. Communication is also important as well, let them know someone is there for them and cares for them.

Another important thing to consider is safety and health risks. Lots of times patients of Alzheimer’s could possibly do something to hurt themselves because sometimes they don’t realize what they are doing at all.

"My advice, as an Alzheimer's care giver, for many years, know and understand the disease so that you can respond to the Alzheimer's victim with patience and compassion. One of the difficulties with living with an Alzheimer's patient is that they get frustrated easily, and your patience will help relieve their frustration and help them to adjust to the change more easily," Cheryl Clines, caregiver and mother of a SCC student said.

It's all in the cortex: After a domestic squabble, brain activity appears to predict resiliency

Research suggests that the brain's lateral prefrontal cortex plays an important role in showing how well someone can rebound emotionally the day after an argument.

Common wisdom says that domestic partners shouldn’t go to bed angry if they want to foster successful relationships. But new research from a psychologist at Harvard University suggests that brain activity — specifically in the region called the lateral prefrontal cortex — is a far better indicator of how someone will feel in the days following a fight with a partner.

Individuals who show more neural activity in the lateral prefrontal cortex are less likely to be upset the day after fighting with partners, according to a study in this month’s Biological Psychiatry. The findings point to the brain area’s role in regulating emotions, and suggest that improved function within this region also may improve day-to-day mood.

“What we found, as you might expect, was that everybody felt badly on the day of the conflict with their partner,” said lead author Christine Hooker, assistant professor of psychology in Harvard’s Faculty of Arts and Sciences. “But the day after, people who had high lateral prefrontal cortex activity felt better, and the people who had low lateral prefrontal cortex activity continued to feel badly.”

Hooker’s co-authors are Özlem Ayduk, Anett Gyurak, Sara Verosky, and Asako Miyakawa, all of the University of California, Berkeley.

Research has previously shown that the lateral prefrontal cortex is associated with emotion regulation in laboratory tests, but the effect has never been proven connected to experiences in day-to-day life.

This study involved healthy couples who have been in relationships for longer than three months. While in an fMRI scanner, participants viewed pictures of their partners with positive, negative, or neutral facial expressions, and their neural activity was recorded while reacting to the images. While in the lab, participants were also tested for their broader cognitive control skills, such as their ability to manage impulses and the shift and focus of attention.

For three weeks, the couples also recorded in an online diary their daily emotional states and whether they had had fights with their partners.

Hooker found that participants who displayed greater activity in their lateral prefrontal cortex while viewing their partner’s negative facial expressions in the scanner were less likely to report a negative mood the day after a fight, indicating they were better able to “bounce back” emotionally after the conflict.

She also found that those who had more activity in the lateral prefrontal cortex and greater emotional regulation after a fight displayed more cognitive control in laboratory tests, indicating a link between emotion regulation and broader cognitive control skills.

“The key factor is that the brain activity in the scanner predicted their experience in life,” said Hooker. “Scientists believe that what we are looking at in the scanner has relevance to daily life, but obviously we don’t live our lives in a scanner. If we can connect what we see in the scanner to somebody’s day-to-day emotion regulation capacity, it could help psychologists predict how well people will respond to stressful events in their lives.”

While Hooker acknowledges that more work must be done to develop clinical applications for the research, it may be that lateral prefrontal cortex function provides information about a person’s vulnerability to develop mood problems after a stressful event. This raises the question as to whether increasing lateral prefrontal cortex function will improve emotion regulation capacity.

Brain Waves Aid Study of Language Impairment

Callier Researcher Hopes Measurements Can Help Improve Therapies
 By looking at how the brain responds to different aspects of grammar, specifically nouns and verbs, researchers at the UT Dallas Callier Center for Communication Disorders are hoping to provide a better understanding of the nature of language disorders in children.
Dr. Diane Ogiela, a post-doctoral fellow at the Callier Center and principal investigator of the study, is using brain waves to study the nature of Specific Language Impairment (SLI) in children. Children with SLI have difficulty in language development while appearing to have otherwise normal cognitive abilities. Grammar is particularly challenging for children with SLI.
“We know that children with a language impairment have difficulty with verbs, which play an important part in developing more complex language skills,” said Ogiela. “By using electroencepholography, also called EEG, we can analyze the brain waves to see how children with language impairment respond to verbs as compared to nouns and to what extent their responses vary from children with typical language.”
To measure the brain waves, the researchers place a cap embedded with sensors on the head of a participant. The participant then listens to recorded sentences that elicit neurological responses to particular nouns and verbs. The researchers then analyze and compare those responses.
“By looking at the neurological response that children have to nouns and verbs, we can see if the brain processes the two types of words with the same speed, with the same part of the brain and with the same level of consistency in both the children with and without language impairment,” said Ogiela.
Ogiela hopes the information collected from the study will be used to develop more focused therapy strategies for addressing grammar problems in children with language impairment.
“Children with language impairment tend to have difficulty expressing themselves and understanding complex language. But with focused therapy that targets the specific problem, they may be able to learn how to compensate for some of those difficulties,” said Ogiela.
Ogiela’s research focusing on children between the ages of 4 and 7 years is funded by a $30,560 grant from the North and Central Texas Clinical and Translational Science Initiative (NCTCTSI) Pilot Grant Award Program.
She has also been awarded a $10,000 New Century Scholars Research Grant from the American Speech-Language-Hearing Foundation to conduct research with 8- to 10-year-olds with and without language impairment on other aspects of grammar.
Parents interested in enrolling their child in either study may contact Dr. Ogiela at diane.ogiela@utdallas.edu or 214-905-3164. The child must be right-handed, be between the ages of 4 and 10, and have either typical language or a language impairment.

Diet, Exercise Can Improve Thinking

Study finds benefits for the mind, not just the body
MONDAY, March 8 (HealthDay News) -- A good diet and regular exercise may help the mind function better, a new study suggests.
"It looks like exercise and diet improve the range of cognitive function," said Patrick Smith, an intern in clinical neuropsychology and a member of a Duke University team reporting the finding online in the March 8 issue of Hypertension. "It helps executive function, learning and psychomotor speed."
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The researchers followed 124 men and women with high blood pressure who were 52 and a minimum of 15 pounds overweight, on average.
Led by James Blumenthal, a professor of psychology and neuroscience at Duke, the study was designed primarily to determine the effect of diet and exercise on blood pressure and included people with mild to moderate high blood pressure.
The mental studies were included because "some previous data linked exercise and diet to better cognitive function," Smith said. The new results verified those findings, he noted.
A third of the participants went about eating and exercising as they usually did. Another third followed the DASH -- Dietary Approaches to Stop Hypertension -- diet, which emphasizes low-fat dairy products, fruits and vegetables, in combination with regular exercise. The final third were in a program that combined the DASH diet with a weight-management program and aerobic exercise.
Two strategies were used in the weight-management program: One centered on reducing portion size and changing habits, such as snacking. The other used an approach called appetite awareness training, which provides guidelines on how much to eat, not just what to eat.
Smith said the exercise part of the program wasn't drastic -- "workouts of 30 minutes three to four times a week, enough to put the heart up to 75 to 80 percent of its maximum rate."
To assess the effects on mental function, the participants were asked to do certain paper-and-pencil tests, such as crossing off specific digits on a page of numbers as quickly as possible.
The group that ate well and exercised regularly had an overall 30 percent improvement in mental function by the end of the four-month period, the researchers noted.
Physical activity does seem to have a direct effect on brain cells, Smith said. "There are neurochemical changes that happen with exercise, he said. There is increased production of brain-derived neurotrophic factor, which stimulates connection with other brain cells, he said, but also there is some evidence that it helps grow new brain cells."
And the combination of good eating and exercise also produced the expected physical advances. Diet-and-exercise participants lost an average of 19 pounds and lowered systolic blood pressure (the higher of the 120/80 reading) by 16 points and diastolic pressure by 10 points by the end of the four-month program.
Some experts believe the study has shortcomings, however. It's a well-done study, but one that has flaws, said Dr. Donald LaVan, a clinical associate professor of medicine at the University of Pennsylvania and a spokesman for the American Heart Association.
"Its entirely too small," LaVan said. "I would call it a keyhole study, suggestive but nothing definitive. Also, it did not have a control group to look at the effect of exercise alone. We need a bigger study with a longer duration and a control group for exercise alone."
Nothing in the study should deter anyone from exercising for the sake of the mind as well as the body, LaVan said.
"Exercise is great," he said. "But how much exercise itself contributes to mental function is not clear."

Old Enemy Might Help to Prevent Alzheimer’s

Lee Goldstein, Robert Moir, Rudy Tanzi

COMMON VILLAIN Bacteria being attacked by beta amyloid, in this image enlarged 18,500 times. 

For years, a prevailing theory has been that one of the chief villains in Alzheimer’s disease has no real function other than as a waste product that the brain never properly disposed of.

The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognizing friends and family.
But now researchers at Harvard suggest that the protein has a real and unexpected function — it may be part of the brain’s normal defenses against invading bacteria and other microbes.
Other Alzheimer’s researchers say the findings, reported in the current issue of the journal PLoS One, are intriguing, though it is not clear whether they will lead to new ways of preventing or treating the disease.
The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph E. Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimer’s disease.
To his surprise, many looked just like genes associated with the so-called innate immune system, a set of proteins the body uses to fight infections. The system is particularly important in the brain, because antibodies cannot get through the blood-brain barrier, the membrane that protects the brain. When the brain is infected, it relies on the innate immune system to protect it.
That evening, after the lab’s usual end-of-the-week beer hour, Dr. Tanzi wandered into the office of a junior faculty member, Robert D. Moir, and mentioned what he had seen. As Dr. Tanzi recalled, Dr. Moir turned to him and said, “Yeah, well, look at this.”
He handed Dr. Tanzi a spreadsheet. It was a comparison of A-beta and a well-known protein of the innate immune system, LL-37. The likenesses were uncanny.
Among other things, the two proteins had similar structures. And like A-beta, LL-37 tends to clump into hard little balls.
In rodents, the protein that corresponds to LL-37 protects against brain infections. People who make low levels of LL-37 are at increased risk of serious infections and have higher levels of atherosclerotic plaques, arterial growths that impede blood flow.
The scientists could hardly wait to see if A-beta, like LL-37, killed microbes. They mixed A-beta with microbes that LL-37 is known to kill — listeria, staphylococcus, pseudomonas. It killed 8 out of 12.
“We did the assays exactly as they have been done for years,” Dr. Tanzi said. “And A-beta was as potent or, in some cases, more potent than LL-37.”
Then the investigators exposed the yeast Candida albicans, a major cause of meningitis, to tissue from the hippocampal regions of brains from people who had died of Alzheimer’s and from people of the same age who did not have dementia when they died.
Brain samples from Alzheimer’s patients were 24 percent more active in killing the bacteria. But if the samples were first treated with an antibody that blocked A-beta, they were no better than brain tissue from nondemented people in killing the yeast.
The innate immune system is also set in motion by traumatic brain injuries and strokes and by atherosclerosis that causes reduced blood flow to the brain, Dr. Tanzi noted.
And the system is spurred by inflammation. It is known that patients with Alzheimer’s disease have inflamed brains, but it has not been clear whether A-beta accumulation was a cause or an effect of the inflammation. Perhaps, Dr. Tanzi said, A-beta levels rise as a result of the innate immune system’s response to inflammation; it may be a way the brain responds to a perceived infection.
But does that mean Alzheimer’s disease is caused by an overly exuberant brain response to an infection?
That’s one possible reason, along with responses to injuries and inflammation and the effects of genes that cause A-beta levels to be higher than normal, Dr. Tanzi said. However, some researchers say that all the pieces of the A-beta innate immune systems hypothesis are not in place.
Dr. Norman Relkin, director of the memory disorders program at NewYork-Presbyterian/Weill Cornell hospital, said that although the idea was “unquestionably fascinating,” the evidence for it was “a bit tenuous.”
As for the link with infections, Dr. Steven T. DeKosky, an Alzheimer’s researcher who is vice president and dean of the University of Virginia School of Medicine, noted that scientists have long looked for evidence linking infections to Alzheimer’s and have come up mostly empty-handed.
But if Dr. Tanzi is correct about A-beta being part of the innate immune system, that would raise questions about the search for treatments to eliminate the protein from the brain.
“It means you don’t want to hit A-beta with a sledgehammer,” Dr. Tanzi said. “It says what we need is the equivalent of a statin for the brain so you can dial it down but not turn it off.” (Dr. Tanzi is a co-founder of two companies, Prana Biotechnology and Neurogenetic Pharmaceutical, that are trying to dial down A-beta.)
Dr. Relkin said that even if A-beta were not part of the innate immune system, it might not be a good idea to remove it all, along with the hard balls of plaque it makes in the brain.
In the past, Dr. Relkin said, scientists assumed “that the pathology was the plaque.” Now, he likens removing plaque to digging up bullets at the Gettysburg battlefield.
The more bullets in an area, the more intense the fighting was. But “digging up bullets will not change the outcome of the battle,” he said. “Most of us don’t believe that removing plaque from the brain is the end-all.”
But other scientists not connected with the discovery said they were impressed by the new findings.
“It changes our thinking about Alzheimer’s disease,” said Dr. Eliezer Masliah, who heads the experimental neuropathology laboratory at the University of California, San Diego. “I don’t think we ever thought about that possibility for A-beta.”
Dr. Masliah is intrigued by the idea that aggregates of A-beta may be killing bacteria and brain cells by the same mechanism. He noted that Dr. Tanzi had a track record of coming up with unusual ideas about Alzheimer’s disease that later turn out to be correct.
“I think he’s onto something important,” Dr. Masliah said.

New Insight on How Fast Nicotine Peaks in the Brain

Nicotine takes much longer than previously thought to reach peak levels in the brains of cigarette smokers, according to new research conducted at Duke University Medical Center.
Traditionally, scientists thought nicotine inhaled in a puff of cigarette smoke took a mere seven seconds to be taken up by the brain, and that each puff produced a spike of nicotine. Using PET imaging, Duke investigators illustrate, for the first time, that cigarette smokers actually experience a steady rise of brain nicotine levels during the course of smoking a whole cigarette.
The findings, scheduled to appear online in the Early Edition of Proceedings of the National Academy of Sciences (PNAS) the week of March 8, could lead to more effective treatments for smoking addiction.
"Previously it was thought that the puff-by-puff spikes of nicotine reaching the brain explained why cigarettes are so much more addictive than other forms of nicotine delivery, like the patch or gum," says Jed Rose, Ph.D., director of the Duke Center for Nicotine and Smoking Cessation Research. "Our work now calls into question whether addiction has to do with the puff-by-puff delivery of nicotine. It may actually depend in part on the overall rate at which nicotine reaches and accumulates in the brain, as well as the unique habit and sensory cues associated with smoking."
Yet, when the researchers compared 13 dependent smokers to 10 non-dependent smokers, they were surprised to find the dependent smokers had a slower rate of nicotine accumulation in the brain. "This slower rate resulted from nicotine staying longer in the lungs of dependent smokers, which may be a result of the chronic effects of smoke on the lungs," surmises Rose.
The difference in rate of nicotine accumulation in the brain doesn't explain why some people become addicted to cigarettes and others don't. "Even if you correct for the speed of delivery, our study showed the non-dependent smokers eventually experienced the same high levels of nicotine in their brain as dependent smokers, yet they did so without becoming dependent. The real mystery is why."
Rose says the absence of addiction in these smokers could be due to genetic differences, differences in the way they smoke, or differences in the psychological effects they derive. "We're still not able to fully explain why these people are able to smoke without becoming addicted."
Despite the questions raised, the study provides important insights into the role of the speed and level of brain nicotine levels, and which receptors in the brain are at work. "Different receptors respond to nicotine at different levels of sensitivity," says Rose. "Knowing the levels of nicotine that are really getting to the brainsmoking." gives us clues as to which receptors are more likely to be important for the dependence-producing effects of cigarette