Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
In situ immunodetection of neuronal caspase-3 activation in Alzheimer disease
Autore:
Selznick, LA; Holtzman, DM; Han, BH; Gokden, M; Srinivasan, AN; Johnson, EM; Roth, KA;
Indirizzi:
Washington Univ, Sch Med,Dept Pathol, Ctr Study Nervous Syst Injury, Alzheimers Dis Res Ctr, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dis Res Ctr, St Louis, MO 63110 USA Washington Univ, Sch Med,Dept Mol Biol & Pharmacol, Ctr Study Nervous SystInjury, Alzheimers Dis Res Ctr, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dis Res Ctr, St Louis, MO 63110 USA Washington Univ, Sch Med,Dept Neurol, Ctr Study Nervous Syst Injury, Alzheimers Dis Res Ctr, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dis Res Ctr, St Louis, MO 63110 USA IDUN Pharmaceut Inc, La Jolla, CA USA IDUN Pharmaceut Inc La Jolla CA USA DUN Pharmaceut Inc, La Jolla, CA USA
Titolo Testata:
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
fascicolo: 9, volume: 58, anno: 1999,
pagine: 1020 - 1026
SICI:
0022-3069(199909)58:9<1020:ISIONC>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
BETA-AMYLOID NEUROTOXICITY; HIPPOCAMPAL-NEURONS; CNS NEURONS; CELL-DEATH; BCL-X; APOPTOSIS; EXPRESSION; BRAIN; DEGENERATION; PROTEIN;
Keywords:
Alzheimer disease; amyloid beta; apoptosis; autophagy; caspase-3; granulovacuolar degeneration;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Roth, KA Washington Univ, Sch Med,Dept Pathol, Ctr Study Nervous Syst Injury, Alzheimers Dis Res Ctr, 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., "In situ immunodetection of neuronal caspase-3 activation in Alzheimer disease", J NE EXP NE, 58(9), 1999, pp. 1020-1026

Abstract

The mechanism by which cells die in Alzheimer disease (AD) is unknown. Several investigators speculate that much of the cell loss may be due to apoptosis, a highly regulated form of programmed cell death. Caspase-3 is a critical effector of neuronal apoptosis and may be inappropriately activated inAD. To address this possibility, we examined cortical and hippocampal brain sections from AD patients, as well as 2 animal models of AD, for in situ evidence of caspase-3 activation. We report here that senile plaques and neurofibrillary tangles in the AD brain are not associated with caspase-3 activation. Furthermore, amyloid beta (AP) deposition in the APPsw transgenic mouse model of ED does not result in caspase-3 activation despite the ability of AP to induce caspase-3 activation and neuronal apoptosis in vitro. ADbrain sections do, however, exhibit caspase-3 activation in hippocampal neurons undergoing granulovacuolar degeneration. Our data suggests that caspase-3 does not have a significant role in the widespread neuronal cell deaththat occurs in AD, but may contribute to the specific loss of hippocampal neurons involved in learning and memory.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 08:49:17