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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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