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The Latest Brain Research

Why gambling when tired is bad; a new autism treatment; the epigenetics of child abuse.
November 18, 2008

Updates from the Society for Neuroscience Conference in Washington, DC:

Don’t Gamble When Sleep-Deprived

That may seem like obvious advice, but new research presented at the conference provides a neurological explanation for why gambling at the end of a 24-hour party binge is such a bad idea. Vinod Venkatraman and his colleagues at Duke studied volunteers as they played a specially designed gambling test, under both normal conditions and after 24 hours of sleep deprivation. Players could choose to make a risky, high-value bet; a smaller and less risky bet; or a bet that minimized potential losses. Sleep-deprived gamblers were more likely to go for the high-risk, high-reward option. Accompanying brain-imaging studies showed that these players had increased activity in the part of the brain that is linked to rewards–the same area that responds to drugs, food, and sex–and decreased activity in the part of the brain that is linked to risk aversion. No wonder casinos want to keep you gambling.

New Drug Being Tested for Autism

Last year, Mark Bear and Gul Dolen, of MIT, published an exciting finding for the autism community: they described correcting many of the symptoms of fragile X syndrome, a genetic disorder that is the most common form of heritable mental retardation and a leading cause of autism, by changing the activity of a specific gene in mice. Drugs that target the same gene are now being tested in humans, Dolen revealed at the conference this week. This is great news, given the lack of existing or even experimental therapies for autism. Dolen declined to give further details on the tests but says she hopes that the same approach will work for more common types of autism, which do not share the gene mutation that underlies fragile X.

To correct fragile X deficits in mice, researchers started with mice that carry the mutation responsible for the disorder and show many of the same symptoms. They then engineered the mice to have lower levels of a receptor called metabotropic glutamate receptor 5 (mGluR5), which improved abnormal brain development and faulty memory and reduced seizures–some of the defining symptoms of the disorder.

Pharma companies have been developing drugs that target this class of receptors, which are involved in the brain’s primary excitatory signaling mechanism, for a number of disorders, including schizophrenia, chronic pain, Parkinson’s, and anxiety. (I wrote a piece on this new drug class several years ago but haven’t heard much about them since then. According to the NIH clinical trials database, none are in publicly funded clinical trials.) Maybe the autism findings will breathe new life into their development.

A Mechanism Underlying the Long-Lasting Effects of Child Abuse

Epigenetics (changes in gene expression not linked to changes in DNA) is definitely a buzzword at this year’s conference. One of the most interesting presentations on this topic examines the role of epigenetics in a well-known phenomenon: the long-term impact of child abuse. Children who were abused have a much higher risk of developing a variety of mental illnesses, including schizophrenia, depression, and bipolar disorder. Tanya Roth and her colleagues at the University of Alabama, in Birmingham, found that baby mice raised by “stressed caretakers,” who mishandled and ignored their charges during the first week of life, experienced changes in gene expression and methylation of the gene for brain-derived neurotrophic growth factor into adulthood. (Methylation is the addition of methyl groups to DNA or the protein it is wrapped around, and it’s one of the major mechanisms of epigenetics. It makes DNA more tightly wound up and thus harder to transcribe.) Roth hopes that the research will allow scientists to find drugs that can reverse the changes.

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