We propose to investigate the immune system in schizophrenics in order to find out if any abnormalities are present in comparison to the appropriate control patients. It has already been determined that some schizophrenic patients with severe tardive dyskinesia (TD) have elevated antibody titers against human acetylcholine receptor. These antibodies against receptor were discovered because it is possible to purify and label the receptor; but the titers, although significant, were low and this may not necessarily implicate acetylcholine receptors in TD or in schizophrenia. These patients had no clinical signs of Myasthenia Gravis. Neuroleptic medication may induce a whole spectrum of autoantibodies either by stimulating cells of the immune system or by acting upon cell membranes in such a way that protein components are rendered antigenic. Such antibodies would be difficult to detect as we do not know the antigens to which they are directed. This possibility will be further explored by measuring antibody subclasses, T-cell subsets, anti-brain antibodies and anti-nuclear antibodies. As neuroleptics are thought to cause TD we will compare drug treated patients with and without TD. The chronic administration of such drugs to rats for as long as 6 months results in an orofacial syndrome which bears resemblance to TD in humans. We will examine the brains of such animals for evidence of anti-neuronal antibodies or lymphocytes in the brain which could be responsible for the neurological changes which cause the dyskinesia.
| Bradley, R J; Edge, M T; Chau, W C (1990) The alpha-neurotoxin erabutoxin b causes fade at the rat end-plate. Eur J Pharmacol 176:11-21 |
