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Titolo:
Amyloid beta-induced neuronal death is bax-dependent but caspase-independent
Autore:
Selznick, LA; Zheng, TS; Flavell, RA; Rakic, P; Roth, KA;
Indirizzi:
Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Pathol, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Mol Biol & Pharmacol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 & Pharmacol, St Louis, MO 63110 USA Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06510 USA Yale Univ New Haven CT USA 06510 Hughes Med Inst, New Haven, CT 06510 USA Yale Univ, Sch Med, Neurobiol Sect, New Haven, CT 06510 USA Yale Univ NewHaven CT USA 06510 Neurobiol Sect, New Haven, CT 06510 USA
Titolo Testata:
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
fascicolo: 4, volume: 59, anno: 2000,
pagine: 271 - 279
SICI:
0022-3069(200004)59:4<271:ABNDIB>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED NEUTRAL PROTEINASE; CEREBELLAR GRANULE NEURONS; PROGRAMMED CELL-DEATH; ENZYME-LIKE PROTEASES; ALZHEIMERS-DISEASE; DNA FRAGMENTATION; IN-VIVO; BCL-X; HIPPOCAMPAL-NEURONS; FAMILY PROTEASES;
Keywords:
Alzheimer disease; amyloid beta; apoptosis; bax; calpain; caspase-3;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
71
Recensione:
Indirizzi per estratti:
Indirizzo: Roth, KA Washington Univ, Sch Med, Dept Pathol, 660 S Euclid Ave,Box 8118,St Louis, MO 63110 USA Washington Univ 660 S Euclid Ave,Box 8118 St Louis MO USA 63110 A
Citazione:
L.A. Selznick et al., "Amyloid beta-induced neuronal death is bax-dependent but caspase-independent", J NE EXP NE, 59(4), 2000, pp. 271-279

Abstract

Fibrillar amyloid beta (A beta) peptides are major constituents of senile plaques in Alzheimer disease (AD) brain and cause neuronal apoptosis in vitro. Bar and caspase-3 have been implicated in the pathogenesis of AD and are components of a well-defined molecular pathway of neuronal apoptosis. To determine whether A beta-induced neuronal apoptosis involves bar and/or caspase-3 activation, we examined the effect of A beta on wild-type, bax-deficient, and caspase-3-deficient telencephalic neurons in vitro. In wild-type cultures. A beta produced time- and concentration-dependent caspase-3 activation, apoptotic nuclear changes. and neuronal death. These neurotoxic effects of A beta were not observed in bax-deficient cultures. Caspase-3 deficiency, or pharmacological inhibition of caspase activity, prevented caspase-3 activation and blocked the appearance of apoptotic nuclear features but not A beta-induced neuronal death. Neither calpain inhibition nor microtubule stabilization with Taxol protected telencephalic neurons from A beta-induced caspase activation or apoptosis. These results have potential implications regarding the underlying pathophysiology of AD and towards AD treatmentstrategies.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/08/20 alle ore 08:48:05