Circulating autoantibodies to neuronal and glial filament proteins in autism

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Abstract

Automunumty may be a pathogenic factor in autism, a behavioral disorder of early childhood onset. Circulating autoantibodies are produced in organ-specific autoimmunity; therefore, we investigated them in the plasma of autistic subjects, mentally retarded (MR) subjects, and healthy controls. Autoantibodies (IgG isotype) to neuron-axon filament protein (anti-NAFP) and glial fibrillary acidic protein (anti-GFAP) were analyzed by the Western immunoblotting technique. We found a significant increase in incidence of anti-NAFP (P = .004) and anti-GFAP (P = .002) in autistic subjects, but not in MR subjects. Clinically, these autoantibodies may be related to autoimmune pathology in autism.

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    Numerous studies reveal autoantibodies in autism, and specifically, brain autoantibodies, as listed in Table 1 [2,5,27–47]. Brain autoantibodies found in autism include autoantibodies to: (1) human neuronal progenitor cells (a biological cell that has a tendency to differentiate into a specific type of cell); (2) MBP; (3) neuron-axon filament protein (NAFP, which provides structural support for axons); (4) brain endothelial cells (a key component of the blood brain barrier); (5) serotonin receptors; (6) GFAP; (7) brain derived neurotrophic factor (BDNF, a member of the neurotrophin family of growth factors); (8) neuronal tissue; (9) myelin associated glycoprotein; and (10) various brain proteins in the cerebellum, hypothalamus, prefrontal cortex, cingulate gyrus, caudate putamen, cerebral cortex and caudate nucleus [2,5,27–47]. Importantly, brain autoantibodies in autism are found to correlate with the severity of the disorder [39,46].

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    Thus, the relevance, if any, of autoantibodies in ASD based on these methodologies remains unclear. Additionally, specific antigen immunoassays have been used to measure autoantibodies in ASD including autoantibodies against target proteins such as glial fibrillary acidic protein (GFAP), myelin basic protein (MBP) and glutamic acid decarboxylase-65 (GAD65) [11–15]. Singh et al. reported that subjects with ASD had a higher prevalence of autoantibodies against GFAP compared to controls [14], yet another group found no association of autoantibodies against GFAP with ASD [11].

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This work was supported in part by private donations to Dr. Singh at the University of Michigan. He thanks undergraduate students Padma Guthikonda, Kathleen Ang, and Tiffany Heutel for laboratory assistance. The authors thank all blood donors for their participation in this project.

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