Biological basis of autism.
Because of its relative inaccessibility, researchers have only recently been able to study the brain
systematically. But with the innovative emergence of new brain imaging tools – computerized tomography (CT),
positron emission tomography (PET), single photon emission computed tomography (SPECT), and magnetic resonance
imaging (MRI), study of the structure and the functioning of the brain can be done.
With the aid of modern technology and the new availability of both normal and autism tissue samples to do
post-mortem studies, researchers will be able to learn much through comparative studies. Post-mortem and MRI
studies have shown that many major brain structures are implicated in autism. This includes the cerebellum,
cerebral cortex, limbic system, corpus callosum, basal ganglia, and brain stem.
It appears that in autism a disorder is found in the structure of the brain, e.g. the little brain(cerebellum).
There is a disorder localized in the frontal lobes. Low blood flow to certain parts of the brain and reduced
numbers of certain brain cells also seem to appear along with autism traits.
An exciting development is the Autism Tissue Program Studies of the postmortem brain with imaging methods will
help us learn why some brains are large, how the limbic system(interconnected system of brain nuclei associated
with basic needs and emotions such as hunger, pain, pleasure, satisfaction, sex, and instinctive motivation)
develops, and how the brain changes as it ages. Tissue samples can be stained and will show which neurotransmitters
are being made in the cells and how they are transported and released to other cells. By focusing on specific brain
regions and neurotransmitters, it will become easier to identify susceptibility genes.
Other research is focusing on the role of neurotransmitters such as serotonin, dopamine, and epinephrine. Problems
are found in the general functioning of the brain as a result of a shortage or excess of neurotransmitters
(dopamine and serotonin). As a result information entering the brain is not correctly processed.
There is a report by Edwin Cook and his colleagues that the first gene of autism relates to processing serotonin in
the brain. In 1990, Dr. Cook said, “the most consistent finding has been over 25% of autistic children and
adolescents are hyperserotonemic. After decades of investigation the mechanism of hyperserotonemia has not been
determined.” Hyperserotonemia is where you have high-elevated serotonin levels.
Only recently researchers at the School of Medicine have discovered in the placenta what may be the earliest marker
for autism, possibly helping physicians diagnose the condition at birth, rather than the standard age of 2 or
older. Current studies are searching for characteristics in children at risk for ASD so that the diagnosis can be
made prior to age 1. The ideal time for diagnosis would be at birth, according to senior author on the study Dr.
Harvey J. Kliman, research scientist in the Department of Obstetrics, Gynecology & Reproductive Sciences at the
School of Medicine. They found that the placentas from ASD children were three times more likely to have
trophoblast (the embryo’s outer layer) inclusions. Kliman and the team identified trophoblast inclusions by
performing microscopic examinations of placental tissues.
“We knew that trophoblast inclusions were increased in cases of chromosome abnormalities and genetic diseases, but
we had no idea whether they would be significantly increased in cases of ASD,” says Kliman. “These results are
consistent with studies by others who have shown that ASD has a clear genetic basis.” Trophoblast inclusions
reflect abnormal folding of microscopic layers in the placenta and appear to result from altered cell growth.
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