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Autism Studies and Related Medical Conditions, January 2009 - TACA

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Cook, E. H., Jr., B. D. Perry, et al. (1993). "Receptor inhibition by immunoglobulins:<br />

specific inhibition by autistic children, their relatives, <strong>and</strong> control subjects." J <strong>Autism</strong><br />

Dev Disord 23(1): 67-78.<br />

Forty-two parents of children with autistic disorder, 15 children with autistic<br />

disorder, 17 siblings of children with autistic disorder, <strong>and</strong> 12 unrelated normal<br />

adult controls were studied to determine if immunoglobulins isolated from their<br />

plasma would inhibit binding of the 5HT1A agonist, [3H]-8-hydroxy-N,N-dipropyl-<br />

2-aminotetralin (DPAT) to 5HT1A receptors in human hippocampal membranes.<br />

There were no significant differences among the means of percentage inhibition<br />

of DPAT binding of parents, children with autistic disorder, siblings, or unrelated<br />

controls. In addition, there were no differences in the proportion of subjects with<br />

> 15% DPAT inhibition among autistic children, their parents, their siblings, or<br />

unrelated controls. Immunoglobulin inhibition was not specific for the 5HT1A<br />

receptor binding site, since immunoglobulins inhibited binding to 5HT2, D1, D2,<br />

<strong>and</strong> alpha 2-adrenergic binding sites. The immunoglobulins isolated from normal<br />

controls inhibited [3H]-rauwolscine binding at alpha 2-adrenergic sites less than<br />

immunoglobulins of children with autistic disorder <strong>and</strong> their parents <strong>and</strong> siblings.<br />

This study did not support the hypothesis that autoantibodies to 5HT1A or 5HT2<br />

receptors are characteristic of autistic disorder.<br />

Cooper, E. L. (2003). "Neuroimmunology of autism: a multifaceted hypothesis." Int J<br />

Immunopathol Pharmacol 16(3): 289-92.<br />

Cortesi, M., E. Alfei, et al. (2007). "Linking autism, regression <strong>and</strong> L<strong>and</strong>au-Kleffner<br />

syndrome: integrative role of nerve growth factor." Med Hypotheses 68(5): 1178-9.<br />

Dalton, P., R. Deacon, et al. (2003). "Maternal neuronal antibodies associated with<br />

autism <strong>and</strong> a language disorder." Ann Neurol 53(4): 533-7.<br />

Neurodevelopmental disorders could be caused by maternal antibodies or other<br />

serum factors. We detected serum antibodies binding to rodent Purkinje cells <strong>and</strong><br />

other neurons in a mother of three children: the first normal, the second with<br />

autism, <strong>and</strong> the third with a severe specific language disorder. We injected the<br />

serum (0.5-1.0 ml/day) into pregnant mice during gestation <strong>and</strong> found altered<br />

exploration <strong>and</strong> motor coordination <strong>and</strong> changes in cerebellar magnetic<br />

resonance spectroscopy in the mouse offspring, comparing with offspring of mice<br />

injected with sera from mothers of healthy children. This evidence supports a<br />

role for maternal antibodies in some forms of neurodevelopmental disorder.<br />

Kern, J. K. (2003). "Purkinje cell vulnerability <strong>and</strong> autism: a possible etiological<br />

connection." Brain Dev 25(6): 377-82.<br />

<strong>Autism</strong> is a neurological disorder of unknown etiology. The onset of the abnormal<br />

growth <strong>and</strong> development within the brain is also not known. Current thought by<br />

experts in autism is that the time of onset is prenatal, occurring prior to 30<br />

weeks gestation. However, autism comprises a heterogeneous population in that<br />

<strong>Autism</strong> <strong>Studies</strong> & <strong>Related</strong> <strong>Medical</strong> <strong>Conditions</strong> – <strong>TACA</strong> © Page 45

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