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Antibodies against a neuron-like (HTB-10 neuroblastoma) cell in children with Tourette syndrome

Background: Similar to the model for Sydenham’s chorea, antineuronal antibodies (ANAb), which develop in response to a preceding streptococcal infection, have been speculated to have a role in the development of Tourette syndrome (TS). Methods: Serum antibodies against the neuron-like HTB-10 neurobl...

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Published in:Biological psychiatry (1969) 1999-09, Vol.46 (6), p.775-780
Main Authors: Singer, Harvey S, Giuliano, Joseph D, Hansen, Bendt H, Hallett, Joseph J, Laurino, Joseph P, Benson, Margaret, Kiessling, Louise S
Format: Article
Language:English
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Summary:Background: Similar to the model for Sydenham’s chorea, antineuronal antibodies (ANAb), which develop in response to a preceding streptococcal infection, have been speculated to have a role in the development of Tourette syndrome (TS). Methods: Serum antibodies against the neuron-like HTB-10 neuroblastoma cell were assayed by ELISA methods and Western blot analysis on 41 children with TS (mean age 11.3 years) and 39 control subjects (mean age 12.1 years). Results: Group comparisons of ELISA assay optical density (OD) showed that mean OD values for serum antibodies were not different [control (mean ± SEM), .506 ± .076; and TS, .584 ± .053 ( p = .38)]. In contrast, median values [.353 in control subjects and .477 in TS subjects ( p = .012)] were significantly different. Western blots identified numerous bands in all TS and control sera with no difference in identified HTB-10 antigens. There was no relationship between the presence of ANAb and age of tic onset, family history, tic severity, attention deficit hyperactivity disorder, or obsessive compulsive disorder. No relationship existed between positive strep titers (ASO ≥ 166 and/or antiDNAaseB ≥ 170) and ANAb determinations or the severity of tics. Conclusions: Children with TS have higher median, but not mean, levels of ANAb, as measured by the HTB-10 neuroblastoma cell membrane assay. This assay system identified antibodies in both control and clinical groups and failed to identify a relationship between antibodies and clinical phenotype or one-time markers for streptococcal infection. Further studies are required to define a possible immune-mediated hypothesis for TS.
ISSN:0006-3223
1873-2402
DOI:10.1016/S0006-3223(98)00384-9