Monday, May 24, 2010

Why Getting Messy Is Good

(Family Features) Playing outside and getting messy may just seem like fun to kids, but playtime actually has an important role in child development. Research shows that various types of play and parental interaction are vital to the healthy development of children. That's why award-winning child care author of "The Big Book of Parenting Solutions," and mom of three, Dr. Michele Borba is teaming up with all® Oxi-Active™ laundry detergent to let moms know it's okay to let their little ones get dirty and have a blast doing it, instead of fretting about the mess.
"By teaching kids that it's okay to get messy sometimes and even encouraging it occasionally, we as parents show them that nobody is perfect, that accidents happen and most importantly, we teach them to be themselves," said Borba. "Childhood is just too short to worry about getting dirty. Moreover, today's advanced detergents, such as all® Oxi-Active, can remove many tough stains in one wash, but the memories that come with making them can last a lifetime."
"We have always known that kids and play are just a natural combo," Borba said. "But new research also shows that letting kids engage in self-directed play has immense value for their social, emotional, cognitive and physical growth."
  • Play expands kids' minds and neurological development. Self-initiated play improves skills such as problem solving and interpreting and is important to brain development and learning.
  • Play boosts children's creativity and imagination. Play gives children the chance to invent, build, expand, explore and develop a whole different part of the brain.
  • Play stretches our children's attention spans. Playing outdoors just 30 minutes a day increases child's ability to focus and pay attention.
  • Play boosts self-confidence and self-regulation. Kids learn to become masters of their own destiny without an adult directing, pushing, managing or scheduling
  • Play helps kids learn to enjoy just being in their own company, entertaining themselves and developing identity. Ease that guilt when your kid says, "I'm bored, Mom!" and wants to be amused by you.
Borba urges parents to ask these questions:
  • How much are your kids plugged into some kind of a digital device? (Did you know the average child is plugged in for 7 1/2 hours a day?)
  • How often are they glued to that TV or clicking that keypad?
  • How much free time do they have (unscheduled, unsupervised)?
  • How often do they go outdoors to just decompress?
  • Do your kids know how to entertain themselves and enjoy the great outdoors?
  • How do you respond when they get messy?

Of Mice and Men - Genetic research and its importance in autism

How does genetic research benefit people living with autism today? And why do scientists do autism research on mice? Those are two of the questions I discussed with researchers at this year's IMFAR autism science conference.

We'll start with genetics, an area of study that's often misunderstood . . .

The available evidence suggests that autism has both genetic and environmental components. When you study autistic minds at the cellular level, it's possible to find many subtle differences between the brain cells and structures of people with autism and our nypical counterparts. Researchers are working hard to look at those differences and why they occur. At first, scientists thought we were born a certain way, but that thinking has evolved. Now most scientists believe our genes give us a predisposition toward something but both genes and the environment shape the final result.

Adding to the complexity of this is that "environment" is a catch-all word for many different things, including the air we breathe, our food, our water, and even the social community where we're parented and raised. We are truly the product of the genetic material we start with and everything we encounter from that point forward.

Researchers have been cataloging autistic differences for some years now. Essentially, they start with the observable manifestation of a difference (like ignoring the people around you, or failing to communicate in the normal ways) and work backward till they find a possible biological reason why. For example, a first clue might be an area of the brain that's too large or too small. Research biologists look at smaller and smaller structures until they get to the smallest difference, which might be an error in the DNA code for those cells.

Having found an abnormal part of the brain, and a possible genetic explanation, they now need to test their ideas out. That's where the mice come in.

You may have read stories about our gene splicing and engineering skills. Genetic engineering has given us many things, from cloned sheep to drought resistant corn. It also gives us a powerful tool to study complex disorders in humans. In these experiments, mice stand in for people.

By introducing the genetic mutations we discover into mice, we are able to observe changes in their brains and even their behavior.

Why mice?

As it happens, mice are uniquely suited for this work. They are genetically very similar to humans, with over 99% similarity in the areas of the brain we're studying in autism research. Almost every human gene has its analogue in a mouse. Mice are also social animals, making it possible to observe the impact of genetic changes in their behavior. Finally, mice grow fast and are relatively inexpensive to raise.

The human genome has about 3.2 billion base pairs, with about 25,000 actual genes. In a stroke of great fortune for scientists, almost every human gene can be found in a mouse. Mice have fewer base pairs than humans, but their gene count is about the same. Researchers can insert actual human DNA into mice genes, and then breed a population of altered mice for study. This sort of work has been extraordinarily valuable to medical science, giving us insights we just couldn't get any other way.

When we introduce a human genetic aberration into a mouse we are able to see for sure whether that change introduces a structural change in the mouse's brain. But more important, we get a chance to learn how such a change impacts the mouse's behavior. Indeed, we are finding genetic differences that do actually translate into autistic behaviors in mice. For example, some differences make normally social mice totally ignore other mice in a cage. Other differences make the mice wring their "hands" and flap in a pattern of behavior that's striking similar to human autistic stimming.

Once scientists have a mouse that exhibits a particular autistic trait, it is then possible to experiment with therapies to correct the problems. That's where we are now with a number of genetic differences associated with autism. We are also able to study the relationship between a genetic difference and the environment with mice.

Some of the best-known examples of this work can already be seen in the grocery store, or the hardware store. Just look at the label warnings that tell you repeated exposure to a certain chemical causes cancer. We see those warning labels on packages everywhere. We identify cancer-causing chemicals by exposing mice to a particular compound and seeing if they develop cancer. In the autism world, researchers have looked at exposure to high levels of lead, mercury, and other chemicals to learn how they affect the developing or developed mouse brain.

One day, thanks to this sort of research, we might have labels that say, "Warning - Exposure to xxxx can cause autism." There may indeed be environmental toxins that trigger autistic regression in people, and there may be chemicals that make autism like mine worse. If I knew what they were I'd be sure to avoid them - any of us would - but science needs to identify them first.

We know some chemicals are dangerous. Most of us already avoid heavy metals and other known toxins. My concern is that we may find other common but currently ignored compounds that are safe for some people but dangerous to others of us on the spectrum. For many of us, that knowledge cannot come soon enough.

On a hopeful note, we can also try various drugs, some of which can minimize or fix damage that started in the genetic code. For example, researchers have recently found that people with autism have excessive brain plasticity. Plasticity is the ability of your brain to change in response to life circumstances. Plasticity is essential to learn new skills, but too much of it can prevent you from learning much at all, because your mind can't "take a set."

We know how to create mice with excess plasticity, and we are now studying the effectiveness of drugs to reduce plasticity in abnormal mice. It's both safer and faster to try these new drug therapies in mice, because they develop so much faster than humans. That work may - hopefully - lead to promising discoveries that can be tested in humans and perhaps ultimately lead to new therapies for that particular component of autism.

It's important to keep in mind that we are not creating "autistic mice." Autism is an extremely complex disorder, to the extent that many people say no two autistic people are the same. What we're doing is modeling specific autistic differences by finding genetic codes that are associated with them.

That sounds easy, but it's not. One problem is that a social behavior - like ignoring your fellow mice - might be associated with more than one genetic difference. In humans, we have hundreds or even thousands of subtle differences associated with autism. And no one genetic difference is common to all of us.

That's why this is such a hard problem to unravel. We can isolate a difference, and even develop a therapy to fix the changes it causes, but that difference may only be present in 1% of the autistic human population. So what do we do for the other 99%? We continue our studies of mice and men, I suppose.

Some people are critical of genetic research in the field of autism, because they fear it may lead to prenatal screening and the abortion of autistic fetuses. Neither of those thoughts had any place in the discussions I had or heard at last week's conference.

Others criticize genetic studies because they think (wrongly) that the work won't benefit anyone living today.

No one can say what the full ramifications of any particular research may be, but I hope the ideas I've shared here make the importance of ongoing genetic research clearer. There is indeed a very good possibility that genetic research today will lead to therapies to mitigate certain components of autistic disability well within our lifetimes.

I sure hope so.

Researchers Report Thymosin Beta 4 Significantly Reduces Damage from Traumatic Brain Injury and Improves Brain Function in Experimental Animals

RegeneRx Biopharmaceuticals, Inc. /quotes/comstock/14*!rgn/quotes/nls/rgn (RGN 0.37, +0.03, +8.82%) announced today that in a preclinical research paper published in the May 2010 issue of the Journal of Neurosurgery, (online ahead of publication), scientists found that the systemic administration of thymosin beta 4, or TB4, significantly reduced brain tissue damage and improved brain function in rats with traumatic brain injury, or TBI. In the study, 10 rats were injected with TB4 one day following the inducement of TBI and four times thereafter over a 12-day period, while 9 rats were injected with a placebo or saline solution. In the group of rats treated with TB4, researchers observed reduced cell loss in the hippocampus, a part of the brain that plays an important role in long-term memory, as compared to the placebo group. The rats treated with TB4 also experienced growth of new blood vessels and neurons in the injured cerebral cortex, growth of brain cells known as oligodendrocytes in the CA3 field of the hippocampus, and recovery of sensory and motor functions as well as spatial learning. The researchers noted that the data for the first time demonstrate that delayed administration of TB4 significantly improves histological and functional outcomes in rats with TBI, indicating that TB4 has considerable therapeutic potential for patients with TBI.
"We believe these results are very encouraging. The fact that TB4 was administered beginning one day following injury and was still able to improve outcomes is significant," added Dr. Allan L. Goldstein, professor of biochemistry and molecular biology at the George Washington University Medical School, and chairman of the board of directors and chief scientific advisor for RegeneRx. "We have now seen compelling data using TB4 in three different animal models -- an EAE mouse model for multiple sclerosis, a rat model for embolic stroke, and this new study in traumatic brain injury -- that have each demonstrated TB4's ability to promote angiogenesis, regenerate neuronal tissue, and improve functional outcome. These data are also consistent with previously published studies showing regeneration of heart tissue after ischemic injuries to the myocardium."
About RegeneRx Biopharmaceuticals, Inc.
RegeneRx is focused on the development of a novel therapeutic peptide, Thymosin beta 4, or TB4, for tissue and organ protection, repair and regeneration. Currently, RegeneRx has formulated three product candidates in clinical development: RGN-352, an injectable formulation for systemic delivery to treat cardiovascular diseases, central nervous system diseases, and other medical indications that require administration by injection, that has completed a Phase 1 clinical trial; RGN-259, a sterile, preservative-free topical eye drop for ophthalmic indications that is currently being supported in compassionate use studies; and RGN-137, a topically applied gel for chronic dermal wounds and reduction of scar tissue that is currently in a Phase 2 clinical trial for the treatment of epidermolysis bullosa. RegeneRx is initially targeting RGN-352 for the treatment of patients who have suffered an acute myocardial infarction, or heart attack, although recent animal research suggests that this formulation may also benefit patients with multiple sclerosis and stroke. RegeneRx has a fourth product candidate, RGN-457, which is an inhaled formulation targeting cystic fibrosis and other pulmonary diseases, in pre-clinical development. These product candidates are based on TB4, a synthetic copy of a 43-amino acid, naturally-occurring peptide that is the subject of an exclusive worldwide license from the National Institutes of Health. In addition to the four pharmaceutical product candidates described above, RegeneRx is pursuing the commercial development of peptide fragments of TB4 for potential cosmeceutical use. RegeneRx holds over 60 worldwide patents and patent applications related to its product candidates.
Forward-Looking Statements
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Eye Test For Alzheimer's?

(Ivanhoe Newswire) ? The protein that forms plaques in the brain in Alzheimer's disease also accumulates in the eyes of people with Down syndrome.

The new findings show that the toxic protein, known as amyloid-ß, that causes Alzheimer's pathology in the brain also leads to distinctive cataracts in the eyes of people with Down syndrome. The discovery is leading the researchers to develop an innovative eye test for early detection of Alzheimer's pathology in both disorders.

The research was led by Lee E. Goldstein, M.D., Ph.D., associate professor at Boston University School of Medicine and the Boston University Alzheimer's Disease Center, and Juliet A. Moncaster, Ph.D., associate director of the Molecular Aging & Development Laboratory, also at Boston University.

"People with Down syndrome develop symptoms of Alzheimer's-type dementia often by the age of 30," senior corresponding author Lee E. Goldstein, was quoted as saying. "This is because they have an extra copy of a key Alzheimer's gene that leads to increased amyloid-ß accumulation in the brain. We discovered that this same protein starts to accumulate very early in the lens of the eye, even in children."

"The lens provides a window to the brain," co-lead author Juliet A. Moncaster was quoted as saying. "The lens can't clear protein deposits the way the brain does. Our findings show that the same amyloid-ß protein that aggregates in the brain also accumulates in the lens and leads to these unusual cataracts in Down syndrome."

"The results are striking," David G. Hunter, M.D., Ph.D., Ophthalmologist-in-Chief at Children's Hospital Boston was quoted as saying. "We have known that these cataracts are prevalent in people with Down syndrome and are sometimes seen at birth, but we never knew how they were related to the disorder—now we know," said Hunter. "These distinctive cataracts appear only in people with advanced Alzheimer's disease and much earlier in Down syndrome."

"We are developing an eye scanner to measure amyloid-ß in the lens," said Goldstein. "This approach may provide a way for early detection and monitoring of related pathology in the brain. Effective treatments for the brain disease in Down syndrome and Alzheimer's disease are on the horizon, and early detection is the key for successful intervention," he said. "The path to effective treatment is what drives our research.

Middle age spread linked to dementia

Middle age spread has been assosciated with higher risks of developing dementia by new research.
Researches have found that a paunch at middle age means that otherwise healthy people are more likely to develop the syndrom assosciated with deterioration of the brain in their old age.

According to the World Health Organisation, an estimated 24.3 million people have some form of dementia with 4.6 million new cases a year.

The study, carried out by the Boston University School of Medicine, has now shown that the disease may be linked to obesity after they found excess weight was assosciated with lower total brain volume.

Dr Sudha Seshadri, who ran the research, said: "Our data suggests a stronger connection between central obesity, particularly the visceral fat component of abdominal obesity, and risk of dementia and Alzheimer's disease."

In the largest study of its kind Dr Seshadri and her colleagues studied over 700 participants who had an average age of 60 and compared their BMI, waist circumferance, waist to hip ratio, CT-based measures of abdominal fat, with MRI measures of total brain volume (TCBV), temporal horn volume (THV), white matter hyperintensity volume (WMHV) and brain infarcts.

She said: "Our results confirm the inverse association of increasing BMI with lower brain volumes in older adults and with younger, middle-aged adults and extends the findings to a much larger study sample."

Dementia, which can be attributed to irreversible causes like Alzheimer's, vascular dementia, or Huntington's disease or caused by treatable conditions such as brain tumours, can cause a decline in short and long term memory, language processing, problem solving capabilities and other cognitive functions.

Clinical diagnosis of dementia is made when two or more brain functions are significantly impaired.

It is hoped that the findings may result promising prevention stratergies in the future.

Dr. Seshadri said: "Our findings, while preliminary, provide greater understanding of the mechanisms underlying the link between obesity and dementia.

"Further studies will add to our knowledge and offer important methods of prevention."

The results of the study have been published in the Annals of Neurology, a journal of the American Neurological Association.

Brain surgery does not stop woman from earning degree

DALLAS - When the twitches and seizures began 12 years ago, Christina Santhouse knew when each one happened. When it was time for a hemispherectomy, where doctors removed half of her brain, she knew the risks and wrote the permission letter for the surgery. When a school counselor said she shouldn't aspire to anything higher than answering phones, she knew the counselor was wrong.
And Santhouse knew she earned her master's degree when she walked across the stage at Misericordia University's commencement on Sunday.
"I think doctors are preprogrammed to tell you what you aren't going to be able to do, not that they ever tried to hold me back, but if I'd listened to them I would never have been able to do all the things I've done," she said.
The 23-year-old speech-language pathology graduate, from Bristol, received one of 558 graduate and undergraduate degrees awarded by Misericordia at its 84th annual commencement.
Hemispherectomy patients often have physical, visual, language and cognitive problems, as they rely on half of their brain. Santhouse said she worked harder, often spending twice as long on studying because she had to use all of her senses to learn by reading and writing notes, saying and hearing lessons.
"I think it just adds to the possibility you can do so much after being damaged, and there are going to be strides and strengths after brain damage," she said.
Santhouse also used her experience in a study with Assistant Professor Hunter Manasco, about life after a hemispherectomy, and helped present it at a national convention.
"She's very much defying the odds," he said. "The best doctors in the world who specialize in this, they attempted to dissuade her from going into speech pathology and the fact she's done as well as she has, it's just a testament to what hard work does."
Hard work and progress were the focus of commencement speaker and former U.S. Ambassador Prudence Bushnell's remarks to the class of 2010. Her efforts to raise warnings about the 1994 Rwandan genocide is captured in the movie "Sometimes in April."
She told the students that as many of them are in the millennial generation, they have much "unfinished business waiting for you," from the retiring baby boomers like herself, and Bushnell strongly emphasized the importance of improving women's rights worldwide, creating collaborative and more equal governments and Americans getting involved internationally to create a better world.
Graduating marketing student Brian Skursky, of West Wyoming, said he's excited to graduate, but feels it is going to be tough to leave a place where he learned so much and spent so much time. The marketing student is taking a job at Mohegan Sun at Pocono Downs as a credit representative.
"I'm thrilled it's over but at the same time, I'm a little upset it's over," he said.
Graduation emotions were also mixed for psychology major Matthew Vitale, of West Pittston, who is heading to graduate school.
"I feel kind of numb to it because I'm going to grad school," he said. "I'm only free for a week and a half, so I guess I'm going to go pack for fun."
Wherever the graduates are headed after Misericordia, student valedictorian Jason Platts, a medical imaging major, sent them with words of encouragement not to take the easy path in life.
"Be confident with your choices and be willing to take a chance because life has a way of working out," he said.

Love on the Global Brain

Brain scan studies have shown that early romantic love generates a unique pattern of brain activity. Regions of the brain related to addiction and even mental illness light up on the scan when a person sees a photo of his or her beloved.
But most of the research has been conducted in Western cultures like Britain and the United States. So researchers at Stony Brook University in New York wanted to know if the chaos of romantic love translates across cultures. For instance, does a Chinese brain look the same as an American brain when it’s in love?
There are reasons to think that culture and country influence how we love — or at least how we express it. For instance, in surveys, people from China typically describe romantic love “in much less positive terms,” notes Art Aron, a professor of psychology at Stony Brook who has conducted several love and brain scan studies.

World's first stem cell project to recreate brain disease news

Scientists in the UK have launched the first stem cell project for the study of a devastating and progressive disease, which affects brain and spinal cord nerves that control muscles in the body.
In the incurable condition, brain and spinal cord nerves that control muscles steadily die off, leaving people paralysed and unable to talk or breathe. Patients can only breathe with the aid of a mechanical ventilator.
The research, which is being led by Sir Ian Wilmut, the Edinburgh-based creator of Dolly the cloned sheep, will use stem cells to make diseased and healthy brain cells, to study how motor neurone disease (MND) progresses into a lethal condition.
The research will open up a window into a condition that is almost impossible to study in living patients and could be the best long-term hope for doctors to find treatments for the condition.
The condition takes a toll of 50 per cent of the patients within three years of a diagnosis and around five deaths are reported from the condition in Britain alone every day. One of the longest-living survivors of the condition is Stephen Hawking, the 68-year cosmologist diagnosed at the age of 21.
Wilmut's team at Edinburgh will work with scientists in London and New York to understand the processes responsible for the death of nerve cells and the spread of the disease to healthy parts of the brain and the central nervous system.