Neurochemical correlates of autistic disorder: A review of the literature
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Date
2006
Journal Title
Journal ISSN
Volume Title
Publisher
Elsevier Ltd.
Abstract
Review of neurochemical investigations in autistic disorder revealed that a wide array of transmitter systems
have been studied, including serotonin, dopamine, norepinephrine, acetylcholine, oxytocin, endogenous
opioids, cortisol, glutamate, and gamma-aminobutyric acid (GABA). These studies have been complicated
by the fact that autism is a very heterogeneous disorder which often presents with comorbid behavioral
problems. In addition, many of these studies employed very small samples and inappropriate control groups,
making it difficult to draw conclusions with confidence. Overall, serotonin appears to have the most empirical
evidence for a role in autism, but this requires further investigation and replication. There is little support for
the notion that a dysfunction of norepinephrine or the endogenous opioids are related to autism. The role of
dopaminergic functioning has not been compelling thus far, though conflicting findings on central dopamine
turnover require further study. Promising new areas of study may include possible dysfunction of the
cholinergic system, oxytocin, and amino acid neurotransmitters. Implications for pharmacotherapy are
briefly discussed for each neurotransmitter system with brief research examples. Review of this work
emphasizes the need for future studies to control for subject variables, such as race, sex, pubertal status, and
distress associated with blood draws, which can affect measures of neurochemical function. In addition,
research in neurochemistry must continue to work in concert with other subspecialties to form a more
comprehensive and theory-based approach to the neurobiological correlates of autistic disorder.
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Citation
Kristen S.L. Lam, Michael G. Aman and L. Eugene Arnold, "Neurochemical correlates of autistic disorder: A review of the literature," Research in Developmental Disabilities 27, no. 3 (2006), doi:10.1016/j.ridd.2005.03.003