Date of Award:

5-1-1994

Document Type:

Thesis

Degree Name:

Master of Science (MS)

Department:

Biology

Department name when degree awarded

Biology

Committee Chair(s)

Reed P. Warren

Committee

Reed P. Warren

Committee

Vijendra K. Singh

Committee

LeGrande C. Ellis

Abstract

Immunological studies of autistic subjects have revealed certain features that are also found in subjects with other autoimmune diseases. Autoantibodies to neural tissue antigens and neurofilament proteins have been implicated in several disease conditions (e. g. autism, Alzheimer's disease, amyotrophic lateral sclerosis, retinitis pigmentosa, spongiform virus encephalopathies, and perhaps other neurological disorders). Sera from patients with these diseases have been examined with immunoblotting, immunofluorescence microscopy, and enzyme-linked-immunosorbent assay and each has found antibodies that react with proteins of neurofilaments. At present, the etiology and pathological mechanisms of most of these diseases are unknown. This study was undertaken to investigate the presence of antibodies reactive with neurofilament proteins in the sera of patients with autism, their household contacts (parents and siblings), healthy controls, and disease controls. Serum samples from 39 autistic subjects, 38 parents of autistics, 26 siblings of autistics, 24 idiopathic mentally retarded subjects, and 58 healthy control subjects were examined for reactivity in immunoblots of partially purified neurofilament preparation from bovine spinal cord. Twenty-five of 39 (64%) of the autistic subjects were reactive with at least one of the neurofilament triplet proteins. The healthy control group had 17 of 58 (29%) reactive for the neurofilament triplet proteins, indicating a significant difference in the presence of antibodies to neurofilament proteins between the two groups. Antibodies to neurofilament proteins were also detected in a significantly high frequency among the household contacts. The detection of autoantibodies to neurofilament proteins substantiates an immune hypothesis involving autoimmunity as one possible mechanism of pathogenesis in a subset of autism. An increase in the incidence of antibodies reactive with glial fibrillary acidic protein (GFAP) was also found in autistic subjects compared with healthy controls. Eight of 39 (20.5%) sera from autistic subjects were reactive with GFAP, while 5 of 58 (8.6%) sera of healthy controls were positive for the same reaction. This finding, upon further investigation, may provide further evidence for the involvement of autoantibodies to neural tissue antigens in autism.

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