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Titolo:
Cortical Bcl-2 protein expression and apoptotic regulation in schizophrenia
Autore:
Jarskog, LF; Gilmore, JH; Selinger, ES; Lieberman, JA;
Indirizzi:
Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 chiat, Chapel Hill, NC 27599 USA Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC 27599 USA Univ NCarolina Chapel Hill NC USA 27599 macol, Chapel Hill, NC 27599 USA Univ N Carolina, Sch Med, Dept Radiol, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 adiol, Chapel Hill, NC 27599 USA Univ N Carolina, Sch Med, Mental Hlth & Neurosci Clin Res Ctr, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 s Ctr, Chapel Hill, NC 27599 USA
Titolo Testata:
BIOLOGICAL PSYCHIATRY
fascicolo: 7, volume: 48, anno: 2000,
pagine: 641 - 650
SICI:
0006-3223(20001001)48:7<641:CBPEAA>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHILDHOOD-ONSET SCHIZOPHRENIA; MATTER VOLUME DEFICITS; ALZHEIMERS-DISEASE; TEMPORAL-LOBE; PREFRONTAL CORTEX; BRAIN-DEVELOPMENT; ELDERLY PATIENTS; MOOD DISORDERS; CELL-DEATH; FOLLOW-UP;
Keywords:
Bcl-2; schizophrenia; apoptosis; neurodegeneration; neurodevelopment; neuroprotection;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Jarskog, LF Univ N Carolina, Sch Med, Dept Psychiat, CB 7160, Chapel Hill,NC 27599 USA Univ N Carolina CB 7160 Chapel Hill NC USA 27599 NC 27599 USA
Citazione:
L.F. Jarskog et al., "Cortical Bcl-2 protein expression and apoptotic regulation in schizophrenia", BIOL PSYCHI, 48(7), 2000, pp. 641-650

Abstract

Background: The etiology of schizophrenia remains unknown; however, a rolefor 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 neurodegenerarive disorders. Given that schizophrenia has certain features of a limited neurodegenerative disorder, it was hypothesized that cortical Bcl-2 expression isincreased in schizophreniaMethods: 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. (C) 2000 Society of Biological Psychiatry.

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Documento generato il 31/03/20 alle ore 04:19:43