Researchers Find Fewer Neurons
in the Amygdala of
Males With Autism
Science
Daily, July 2006
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Researchers at the University of
California, Davis, M.I.N.D. Institute have discovered that the
brains of males with autism have fewer neurons in the amygdala,
a part of the brain involved in emotion and memory. The study,
published in the July 19 issue of the Journal of Neuroscience,
is the first neuroanatomical study to quantify a key difference
in the autistic amygdala.
David Amaral, research director of the UC Davis M.I.N.D.
Institute, and former graduate student Cynthia Mills Schumann
counted and measured representative samples of neurons in the
amygdala of nine postmortem brains of males who had autism and
10 postmortem brains of males who did not have autism. Both
subject groups ranged in age from 10-to-44 years at the time of
death. Using a technique known as “unbiased stereological
analysis,” Schumann and Amaral counted neurons using a
computer-aided microscope system. They found significantly fewer
neurons — cells responsible for creating and transmitting
electrical impulses — in the whole amygdala and its lateral
nucleus in the brains of people with autism.
“This is the first quantitative evidence of an abnormal number
of neurons in the autistic amygdala and the first study to use
modern unbiased sampling techniques for autism research,” Amaral
said.
“While we have known that autism is a developmental brain
disorder, where, how and when the autistic brain develops
abnormally has been a mystery,” said Thomas R. Insel, a
physician and director of the National Institute of Mental
Health . “This new finding is important because it demonstrates
that the structure of the amygdala is abnormal in autism. Along
with other findings on the abnormal function of the amygdala,
research is beginning to narrow the search for the brain basis
of autism.”
Now affecting 1 in every 166 children and primarily affecting
males, autism is a lifelong neurodevelopmental disorder
characterized by social and communication deficits. While autism
has clear behavioral indicators, the neural alterations leading
to the deficits have been difficult to pinpoint. In studies
dating back to the mid-1980s, researchers began focusing on the
amygdala because of its importance in generating appropriate
emotional responses and assimilating memories that are key to
social learning — functions that are impaired by autism.
“Previous magnetic resonance imaging studies from several
laboratories, including the M.I.N.D. Institute, have indicated
precocious enlargement of the amygdala in young children with
autism,” said Schumann, who is now a postdoctoral researcher at
the UC San Diego School of Medicine. “But these studies were not
able to determine whether the number of neurons were different
in the autistic amygdala.”
Interpreting these earlier qualitative studies was hampered
because many postmortem brains available for research were from
individuals who had autism as well as epilepsy, a condition
known to cause pathology of the amygdala.
“Back when these studies were conducted, it wasn't easy to
acquire the brain of a deceased person who just had autism,”
Amaral explained. “We are fortunate now to have the Autism
Tissue Program, funded by the National Alliance for Autism
Research and the National Institutes of Health. With their help,
we were able to analyze more than double the number of
previously examined postmortem brains, none of which had seizure
disorders or any major neurological disorder other than autism.”
“A better understanding of the neurobiology of the amygdala is
crucial to advance autism research, and this study helps answer
many important questions about the fundamental basis of autism,”
said Andy Shih, chief science officer for the National Alliance
for Autism Research, which is now merged with Autism Speaks.
“Autism Speaks and the Autism Tissue Program were proud to
support this project so that these important discoveries could
be made.”
By counting the actual number of neurons in tissue samples, the
researchers also overcame a methodological concern raised by
studies that described changes in neuronal density, or neurons
per unit volume, in portions of the amygdala.
“Differences in neuron density could just indicate changes in
tissue volume rather than changes in total cell number. The only
way to determine the actual difference is to systematically
count samples of neurons in a defined volume,” Amaral said.
With this latest confirmation that the amygdala is pathological
in autism, Amaral and colleagues will now determine why there
are fewer neurons in the amygdala and if other parts of the
brain are similarly affected.
“We need to look at other brain regions to find out if the cell
loss is idiosyncratic to the amygdala or a more general
phenomenon,” he said. “We're in the very early stages of
understanding autism and its neurological pathologies. It's
clearly a process with many steps, and at least we are now one
step further.”
Additional research will also help identify the developmental
point in time at which the neuron reduction actually occurs,
which the current study does not address.
“One possibility is that there are always fewer neurons in the
amygdala of people with autism. Another possibility is that a
degenerative process occurs later in life and leads to neuron
loss. More studies are needed to refine our findings,” said
Schumann.
Schumann and Amaral's research was funded by the National
Alliance for Autism Research and the National Institutes of
Health. A copy of the article, “Stereological Analysis of
Amygdala Neuron Number in Autism,” is available from Caitlin
Quigley in the Society for Neuroscience Public Information
Department. She can be reached at (202) 962-4000 or
cquigley@sfn.org.
The UC Davis M.I.N.D. (Medical Investigation of
Neurodevelopmental Disorders) is a unique, collaborative center
bringing together parents, scientists, clinicians and educators
for research on autism, fragile X syndrome, learning
disabilities and other neurodevelopmental disorders. For more
information, visit
www.mindinstitute.org.
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