Biochemical Findings in ASD
Serotonin dysfunction has been implicated as a
possible factor in the genesis of autistic disorder since the finding of
significantly elevated whole blood 5-HT in these patients. Hyperserotonemia is
a robust finding in autistic disorder and has been consistently replicated.
In nonautistic children, serotonin synthesis
capacity, as measured by positron emission tomography (PET), is more than 200%
adult levels until the age of 5, when it begins to decline toward adult levels;
in autistic children, however, serotonin syn-thesis capacity has been shown to
increase gradually between the ages of 2 and 15, reaching a level of 1.5 times
normal adult levels (Chugani et al.,
1999). In related studies others have shown that platelet serotonin levels
appear to stabilize after the age of 12 (Ritvo et al., 1971).
Hyperserotonemia in autistic disorder appears to
have a familial component Several studies have shown that whole blood serotonin
levels have a positive correlation between probands with autism and their
parents and siblings (Leventhal et al.,
1990). Additionally, individuals with autism who have siblings with au-tism
have higher platelet serotonin than autistic subjects without an autistic
sibling, suggesting that hyperserotonemia may be an indicator of autism with a
higher risk of sibling recurrence (Cook and Leventhal, 1996).
It is clear that it is serotonin within platelets
that is respon-sible for the findings of increased whole blood
hyperserotonemia. More than 99% of whole blood serotonin is contained in
platelets, and platelet-poor plasma ultrafiltrate serotonin levels are not
el-evated in subjects with hyperserotonemia. This suggests that pa-tients with
autism exhibit either increased serotonergic uptake in platelets, or decreased
serotonergic release from platelets, leading to an increased steady-state level
of serotonin. There is evidence for a positive correlation between platelet
serotonin levels and the rate of platelet serotonin transport.
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