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. 2000 Oct 1;48(7):641-50.
doi: 10.1016/s0006-3223(00)00988-4.

Cortical bcl-2 protein expression and apoptotic regulation in schizophrenia

L F Jarskog  1 , J H Gilmore, E S Selinger, J A Lieberman
Affiliations

Cortical bcl-2 protein expression and apoptotic regulation in schizophrenia

L F Jarskog et al. Biol Psychiatry. .

Abstract

Background: The etiology of schizophrenia remains unknown; however, a role for apoptosis has been hypothesized. Bcl-2 is a potent inhibitor of apoptosis and also exerts neurotrophic activity in the central nervous system (CNS). Bcl-2 expression is increased in the CNS of several neurodegenerative disorders. Given that schizophrenia has certain features of a limited neurodegenerative disorder, it was hypothesized that cortical Bcl-2 expression is increased in schizophrenia.

Methods: Postmortem temporal cortex was obtained from the Stanley Foundation Neuropathology Consortium with matched control, schizophrenic, bipolar, and depressed subjects. Bcl-2 protein was measured by enzyme-linked immunoassay (ELISA) and Western blot. Primary analysis was limited to schizophrenia versus control subjects.

Results: The ELISA demonstrated 25% less Bcl-2 protein in schizophrenia (p =.046), supported by Western blot results. A secondary analysis of schizophrenic and bipolar subjects revealed twofold higher mean Bcl-2 in antipsychotic-treated versus neuroleptic-naive subjects.

Conclusions: Contrary to our hypothesis, cortical Bcl-2 was reduced in schizophrenia. This supports the notion that schizophrenia is not a classic neurodegenerative disorder; however, less Bcl-2 protein may signal neuronal vulnerability to proapoptotic stimuli and to neuronal atrophy. Also, the association between neuroleptic exposure and higher Bcl-2 levels could underlie the favorable long-term outcomes of patients who receive maintenance antipsychotic treatment.

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