[Adta] Fw: COMMON GENE VERSION OPTIMIZES THINKING -- BUT WITH A POSSIBLE DOWNSIDE

[Cynthia BERROL]

Barbara, 

As always, somevery interesting information here,

Thank you,
 
Cynthia


--- Barbara A Busse <busse002 at mc.duke.edu> wrote:

> 
> Thought this was very interesting.  Barbara Busse
> ----- Forwarded by Barbara A Busse/MCLibrary/mc/Duke
> on 02/12/2007 10:45 AM
> -----
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>              H.GOV>                    COMMON GENE
> VERSION OPTIMIZES       
>                                        THINKING --
> BUT WITH A POSSIBLE     
>                                        DOWNSIDE     
>                       
>              02/09/2007 09:24                       
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> 
> 
> U.S. Department of Health and Human Services
> NATIONAL INSTITUTES OF HEALTH
> NIH News
> National Institute of Mental Health (NIMH)
> <http://www.nimh.nih.gov/>
> 
> EMBARGOED FOR RELEASE: Thursday, February 8, 2007,
> 5:00 p.m. ET
> 
> CONTACT: Jules Asher, NIMH press office,
> 301-443-4356, <e-mail:
> NIMHpress at nih.gov>
> 
> COMMON GENE VERSION OPTIMIZES THINKING -- BUT WITH A
> POSSIBLE DOWNSIDE
> 
> Most people inherit a version of a gene that
> optimizes their brain's
> thinking circuitry, yet also appears to increase
> risk for schizophrenia*, a
> severe mental illness marked by impaired thinking,
> scientists at the
> National Institutes of Health's (NIH) National
> Institute of Mental Health
> (NIMH) have discovered.  The seeming paradox emerged
> from the first study
> to explore the effects of variation in the human
> gene for a brain master
> switch, DARPP-32.
> 
> The researchers identified a common version of the
> gene and showed how it
> impacts the way two key brain regions exchange
> information, affecting a
> range of functions from general intelligence to
> attention.
> 
> Three fourths of subjects studied had at least one
> copy of the version that
> results in more efficient filtering of information
> processed by the brain's
> executive hub, the prefrontal cortex. However, the
> same version was also
> more prevalent among people who developed
> schizophrenia, a severe mental
> illness marked by delusions, hallucinations and
> impaired emotion that
> affects one percent of the population.
> 
> "We have found that DARPP-32 shapes and controls a
> circuit coursing between
> the human striatum and prefrontal cortex that
> affects key brain functions
> implicated in schizophrenia, such as motivation,
> working memory and reward
> related learning," explained Andreas
> Meyer-Lindenberg, M.D.
> 
> "Our results raise the question of whether a gene
> variant favored by
> evolution, that would normally confer advantage, may
> translate into a
> disadvantage if the prefrontal cortex is impaired,
> as in schizophrenia,"
> added Daniel Weinberger, M.D. "Normally, enhanced
> cortex connectivity with
> the striatum would provide increased flexibility,
> working memory capacity
> and executive control. But if other genes and
> environmental events conspire
> to render the cortex incapable of handling such
> information, it could
> backfire -- resulting in the neural equivalent of a
> superhighway to a
> dead-end."
> 
> Meyer-Lindenberg, Weinberger and colleagues in the
> NIMH Genes, Cognition
> and Psychosis program report their results in the
> February 9, 2007 issue of
> the "Journal of Clinical Investigation".
> 
> Previous studies in animals over two decades, most
> notably by Nobel
> Laureate and NIMH grantee Paul Greengard, M.D.,
> Rockefeller University, had
> established that DARPP-32 in the striatum switches
> streams of information
> from multiple brain chemical systems for processing
> by the cortex. Both the
> neurotransmitter that it works through, dopamine,
> and the chromosomal site
> of its gene have been implicated in schizophrenia.
> 
> "Although several groups have looked for possible
> clinical relevance of
> DARPP-32, they have not met with great success,"
> noted Greengard. "This
> study shows a strong connection between this
> molecule and human cognition
> -- and perhaps with schizophrenia."
> 
> "These first glimpses of DARPP-32 at work in the
> living human brain build
> on a quarter century of investigations by
> Greengard's team that ultimately
> linked this pivotal protein to depression and
> substance abuse as well as to
> schizophrenia," added NIMH Director Thomas Insel,
> M.D.
> 
> To understand DARPP-32's role in the human brain,
> the NIMH researchers used
> genetic, structural and functional magnetic
> resonance imaging, and
> post-mortem techniques to identify the human gene's
> variants and their
> functional consequences. Seventy five percent of
> subjects had the most
> common version of the gene, which boosted circuit
> activation, structural
> and functional connectivity and performance on
> thinking tasks, likely by
> increasing gene expression. In 257 affected
> families, people with
> schizophrenia were more likely to have this common
> version of the DARPP-32
> gene.
> 
> Also participating in the study were: Richard
> Straub, Barbara Lipska, Beth
> Verschinski, Terry Goldberg, Joseph Callicott,
> Michael Egan, Stephen
> Huffaker, Venkata Mattay, Bhaskar Kolachana, Joel
> Kleinman, NIMH.
> 
> The National Institute of Mental Health (NIMH)
> mission is to reduce the
> burden of mental and behavioral disorders through
> research on mind, brain,
> and behavior. More information is available at the
> NIMH website <
> http://www.nimh.nih.gov>.
> 
> The National Institutes of Health (NIH) -- The
> Nation's Medical Research
> Agency -- includes 27 Institutes and Centers and is
> a component of the U.S.
> Department of Health and Human Services. It is the
> primary federal agency
> 
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