f**d
发帖数: 768 | 1 ScienceDaily (May 2, 2011) — In 2005, researchers from the University
of North Carolina at Chapel Hill found that 2-year-old children with
autism have brains up to 10 percent larger than children of the same age
without autism.
Now a follow-up study by UNC researchers has found that the children who
had enlarged brains at age 2 continued to have enlarged brains at
ages 4 and 5, but the amount of the enlargement was to the same degree
found at age 2. This increased brain growth did not continue beyond 2
years of age and the changes detected at age 2 were due to overgrowth
prior to that time point. In addition, the study found that the cortical
enlargement was associated with increased folding on the surface of the
brain (or increased surface area) and not an increase in the
thickness of outer layer of the brain (or gray matter).
"Brain enlargement resulting from increased folding on the surface of
the brain is most likely genetic in origin and a result of an increase
in the proliferation of neurons in the developing brain," said Heather
Cody Hazlett, PhD, assistant professor in the Department of Psychiatry,
who is the lead author of the new study, which is published in the
May 2011 issue of Archives of General Psychiatry.
In both the 2005 study and the new study, Hazlett and colleagues
analyzed magnetic resonance imaging (MRI) scans of the children's brains
using computer software developed for that purpose by Martin Styner,
PhD, an assistant professor of computer science and psychiatry at UNC,
and Guido Gerig, PhD, formerly at UNC and now at the University of
Utah.
"From earlier work by our group on head circumference or head size in
children with autism, we think that brain overgrowth in many children
with autism may actually be happening around the first birthday.
Together these findings suggest that we should be searching for genes
that may underlie the over-proliferation of neurons in this early
post-natal period," said Joseph Piven, MD, senior author of the new
study and director of the Carolina Institute for Developmental
Disabilities.
UNC is currently leading two separate studies aimed at that goal.
Hazlett leads the Brain Development in School Age Children with Autism
study, which is funded by Autism Speaks. "It was important to continue
to follow these children to track their brain development to see if
the brain and behavioral differences we observed were maintained as
the children matured," said Hazlett.
UNC is also leading the Infant Brain Imaging Study (IBIS), a National
Institutes of Health-funded multi-center study which includes four sites
around the U.S. "We are studying infant children at high genetic risk
for autism, by virtue of their having an older brother or sister with
autism -- somewhere around 20 percent of those children will develop
autism. We are doing brain scans and behavior assessments on those
children at 6, 12 and 24 months of age to look at how the brain develops
in the subgroup that develop autism before they have symptoms of autism
at 6 months of age and over the interval that they develop autism --
between 6 and 24 months of age, in most cases," Piven said. "We are also
looking at whether specific gene alterations may be responsible."
More information about IBIS is available at http://www.ibisnetwork.
org/.
Authors of the May 2011 article in Archives of General Psychiatry, in
addition to Hazlett, are Michele Poe, PhD, Guido Gerig, PhD, Martin
Styner, PhD, Chad Chappell, Rachel Gimpel Smith, Clement Vachet, MS, and
Piven.
The UNC authors are all affiliated with one or more of the following:
The Department of Psychiatry in the School of Medicine, the Carolina
Institute for Developmental Disabilities, the Frank Porter Graham
Child Development Institute, and the Department of Computer Science in
the College of Arts and Sciences.
1.Heather Cody Hazlett; Michele D. Poe; Guido Gerig; Martin Styner; Chad
Chappell; Rachel Gimpel Smith; Clement Vachet; Joseph Piven. Early
Brain Overgrowth in Autism Associated With an Increase in Cortical
Surface Area Before Age 2 Years. Arch Gen Psychiatry, 2011; 68 (5):
467-476 DOI: 10.1001/archgenpsychiatry.2011.39 |
|
