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Autism Studies and Related Medical Conditions, January 2009 - TACA

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parents report either that their child was abnormal from birth, or that their child<br />

was developmentally normal until sometime after birth, at which time the child<br />

began to regress or deteriorate. Anecdotal reports suggest that some children<br />

with autism have significant illness or clinical events prior to the development of<br />

autistic symptoms. Conceivably, these children may become autistic from<br />

neuronal cell death or brain damage sometime after birth as result of insult. To<br />

support this theory is that marked Purkinje cell loss, the most consistent finding<br />

in the autistic disorder, can result from insult. Evidence suggests that the<br />

Purkinje cell is selectively vulnerable. This article discusses a theory that the<br />

selective vulnerability of the Purkinje cell may play a role in the etiology of<br />

autism, <strong>and</strong> suggests that a future direction in autism research may be to<br />

investigate the possibility of neuronal cell loss from insult as a cause of autism.<br />

Results of a small pilot survey are also discussed.<br />

Kirkman, N. J., J. E. Libbey, et al. (2008). "How Relevant are GFAP Autoantibodies in<br />

<strong>Autism</strong> <strong>and</strong> Tourette Syndrome?" J <strong>Autism</strong> Dev Disord 38(2): 333-41.<br />

Controversy exists over the role of autoantibodies to central nervous system<br />

antigens in autism <strong>and</strong> Tourette Syndrome. We investigated plasma<br />

autoantibody titers to glial fibrillary acidic protein (GFAP) in children with classic<br />

onset (33) <strong>and</strong> regressive onset (26) autism, controls (25, healthy age- <strong>and</strong><br />

gender-matched) <strong>and</strong> individuals with Tourette Syndrome (24) by enzyme-linked<br />

immunosorbent assays. We found a significant difference in autoantibody titers<br />

to GFAP, not accounted for by age, between the Tourette (significantly lower)<br />

<strong>and</strong> regressive autism groups. However, no differences were found between:<br />

classic/regressive; classic/controls; classic/Tourette; regressive/controls; or<br />

controls/Tourette. Autoantibody responses against GFAP are unlikely to play a<br />

pathogenic role in autism or Tourette Syndrome.<br />

Kozlovskaia, G. V., T. P. Kliushnik, et al. (2000). "[Nerve growth factor auto-antibodies<br />

in children with various forms of mental dysontogenesis <strong>and</strong> in schizophrenia high risk<br />

group]." Zh Nevrol Psikhiatr Im S S Korsakova 100(3): 50-2.<br />

The level of autoantibodies (AAb) to nerve growth factor was evaluated in blood<br />

serum of 163 children with different forms of mental dysontogenesis of<br />

endogenic, residual-organic, psychogenic <strong>and</strong> deprivative origin. Significant<br />

elevation of the level of AAb was found in all forms of psychic dysontogenesis.<br />

The most significant elevation of the level of AAb (p < 0.01), as compared with<br />

the controls (45 children), was characteristic for endogenic forms of<br />

dysontogenesis (schizophrenia, early children's autism, schizotypic diathesis).<br />

The level of AAb was also found as an indicator of the acuteness of the<br />

pathologic state. Besides, its elevation was observed 1-2 weeks prior to the<br />

onset of the clinical exacerbation. Elevation of AAb level was also found in<br />

psychic dysontogenesis of residual-organic nature (children with perinatal<br />

encephalopathy), but it was not so significant as compared with the controls (p<br />

< 0.05%). The analysis in the age dynamics of children from this group<br />

<strong>Autism</strong> <strong>Studies</strong> & <strong>Related</strong> <strong>Medical</strong> <strong>Conditions</strong> – <strong>TACA</strong> © Page 46

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