[net-gold] PSYCHOLOGY: DISORDERS: AUTISM : MEDICAL: BRAIN: DISORDERS: Autism Blurs Distinctions Between Brain Regions
- From: "David P. Dillard" <jwne@xxxxxxxxxx>
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- Date: Sun, 21 Aug 2011 11:10:53 -0400 (EDT)
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PSYCHOLOGY: DISORDERS: AUTISM :
MEDICAL: BRAIN: DISORDERS:
Autism Blurs Distinctions Between Brain Regions
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Date: Thu, 2 Jun 2011 17:24:49 -0400
From: "NIH OLIB (NIH/OD)" <olib@xxxxxxxxxx>
To: NIHPRESS@xxxxxxxxxxxx
Subject: Autism Blurs Distinctions Between Brain Regions
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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/>
For Immediate Release: Thursday, June 2, 2011
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CONTACT: Jules Asher, NIMH press office, 301-443-4536,
<e-mail:NIMHpress@xxxxxxx>
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AUTISM BLURS DISTINCTIONS BETWEEN BRAIN REGIONS
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Erodes molecular identities in cortex - NIH-funded study
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Autism
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http://www.nimh.nih.gov/health/topics/autism-spectrum-disorders-
pervasive-developmental-disorders/index.shtml
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blurs the molecular differences that normally distinguish different brain
regions, a new study suggests. Among more than 500 genes that are normally
expressed at significantly different levels in the front versus the lower
middle part of the brain's outer mantle, or cortex, only 8 showed such
differences in brains of people with autism, say researchers funded in
part by the National Institutes of Health.
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"Such blurring of normally differentiated brain tissue suggests strikingly
less specialization across these brain areas in people with autism,"
explained Daniel Geschwind, M.D., Ph.D., of the University of California,
Los Angeles, a grantee of the NIH's National Institute of Mental Health.
"It likely reflects a defect in the pattern of early brain development."
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He and his colleagues published their study online May 26, 2011 in the
journal Nature. The research was based on postmortem comparisons of brains
of people with the disorder and healthy controls.
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In fetal development, different mixes of genes turn on in different parts
of the brain to create distinct tissues that perform specialized
functions. The new study suggests that the pattern regulating this gene
expression goes awry in the cortex in autism, impairing key brain
functions.
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"This study provides the first evidence of a common signature for the
seemingly disparate molecular abnormalities seen in autism," said NIMH
director Thomas R. Insel, M.D. "It also points to a pathway-based
framework for understanding causes of other brain disorders stemming from
similar molecular roots, such as schizophrenia
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http://www.nimh.nih.gov/health/topics/schizophrenia/index.shtml
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and ADHD
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http://www.nimh.nih.gov/health/topics/attention-deficit-
hyperactivity-disorder-adhd/index.shtml
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In an earlier study
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http://www.nimh.nih.gov/science-news/2008/genes-that-turn-on-together-
hold-secrets-of-brains-molecular-instructions.shtml
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the researchers showed that genes that turn on and off together at the
same time hold clues to the brain's molecular instructions. These modules
of co-expressed genes can reveal genetic co-conspirators in human illness,
through what Geschwind and colleagues call "guilt by association." A gene
is suspect if its expression waxes and wanes in sync with others in an
illness-linked module.
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Using this strategy, the researchers first looked for gene expression
abnormalities in brain areas implicated in autism -- genes expressed at
levels different than in brains of healthy people. They found 444 such
differently expressed genes in the cortexes of postmortem brains of people
with autism.
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Most of the same genes turned out to be abnormally expressed in the
frontal cortex as in the temporal cortex (lower middle) of autistic
brains. Of these, genes involved in synapses, the connections between
neurons, tended to be under-expressed when compared with healthy brains.
Genes involved in immune and inflammatory responses tended to be
over-expressed. Significantly, the same pattern held in a separate sample
of autistic and control brains examined as part of the study.
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Autistic and healthy control brains were similarly organized -- modules of
co-expressed genes correlated with specific cell types and biological
functions.
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Yet normal differences in gene expression levels between the frontal and
temporal cortex were missing in the modules of autistic brains. This
suggests that the normal molecular distinctions -- the tissue differences
-- between these regions are nearly erased in autism, likely affecting how
the brain works. Strikingly, among 174 genes expressed at different
levels between the two regions in two healthy control brains, none were
expressed at different levels in brains of people with autism.
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An analysis of gene networks revealed two key modules of co-expressed
genes highly correlated with autism.
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One module was made up of genes in a brain pathway involved in neuron and
synapse development, which were under-expressed in autism. Many of these
genes were also implicated in autism in previous, genome-wide studies
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http://www.nimh.nih.gov/science-news/2008/autism-gene-scans-
converge-on-two-suspect-sites-two-types-of-genetic-risk.shtml
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So, several different lines of evidence now converge, pointing to genes in
this M12 module (see picture below) as genetic causes of autism.
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A second module of co-expressed genes, involved in development of other
types of brain cells, was over-expressed in autism. These were determined
not to be genetic causes of the illness, but likely gene expression
changes related to secondary inflammatory, immune, or possible
environmental factors involved in autism.
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This newfound ability to see genes in the context of their positions in
these modules, or pathways, provides hints about how they might work to
produce illness, according to Geschwind and colleagues. For example, from
its prominent position in the M12 module, the researchers traced a
potential role in creating defective synapses to a gene previously
implicated in autism.
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Follow-up studies should explore whether the observed abnormalities in the
patterning of gene expression might also extend to other parts of the
brain in autism, say the researchers.
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The mission of the NIMH is to transform the understanding
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About the National Institutes of Health (NIH): 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. NIH is the primary
federal agency conducting and supporting basic, clinical, and
translational medical research, and is investigating the causes,
treatments, and cures for both common and rare diseases. For more
information about NIH and its programs, visit
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http://www.nih.gov
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REFERENCE:
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Transcriptomic analysis of autistic brain reveals convergent molecular
pathology
http://www.ncbi.nlm.nih.gov/pubmed/21614001>
Voineagu I, Wang X, Johnston P, Lowe JK, Tian Y, Horvath S, Mill J,
Cantor RM, Blencowe BJ, Geschwind DH.
Nature.
2011 May 25.
[Epub ahead of print] PMID:21614001
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IMAGE INFORMATION:
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URL -
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http://www.nimh.nih.gov/images/news-items/autism-genes.jpg
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Caption -
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A module of co-expressed genes that code for neurons and their connections
tend to be under-expressed in many individuals with autism (red), compared
to controls (gray).
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Alt tag -
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Graph displaying genetic differences of autism
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##
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This NIH News Release is available online at:
http://www.nih.gov/news/health/jun2011/nimh-02.htm
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Sincerely,
David Dillard
Temple University
(215) 204 - 4584
jwne@xxxxxxxxxx
http://daviddillard.businesscard2.com
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