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Titolo:
Caspases, apoptosis, and Alzheimer disease: Causation, correlation, and confusion
Autore:
Roth, KA;
Indirizzi:
Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 l & Immunol, St Louis, MO 63110 USA
Titolo Testata:
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
fascicolo: 9, volume: 60, anno: 2001,
pagine: 829 - 838
SICI:
0022-3069(200109)60:9<829:CAAADC>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; AMYLOID PRECURSOR PROTEIN; NEURONAL APOPTOSIS; DNA FRAGMENTATION; TRANSGENIC MICE; MOUSE MODEL; IN-SITU; NEURODEGENERATIVE DISORDERS; NEUROFIBRILLARY TANGLES; HIPPOCAMPAL-NEURONS;
Keywords:
autophagy; Bcl-2; cathepsin D; neurodegenerative disease; programmed cell death;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
84
Recensione:
Indirizzi per estratti:
Indirizzo: Roth, KA Washington Univ, Sch Med, Dept Pathol & Immunol, 660 S Euclid Ave,Box 8118, St Louis, MO 63110 USA Washington Univ 660 S Euclid Ave,Box 8118St Louis MO USA 63110 A
Citazione:
K.A. Roth, "Caspases, apoptosis, and Alzheimer disease: Causation, correlation, and confusion", J NE EXP NE, 60(9), 2001, pp. 829-838

Abstract

Extensive neuron loss occurs in Alzheimer disease (AD) brain and some authors have speculated that dysregulation of apoptotic death pathways is etiologically responsible for the disease. Apoptosis is regulated in mammalian cells by a family of cysteine proteases called caspases. At least 7 different caspases (caspases 1, 2, 3, 6, 8, 9, and 12) have been implicated in regulating neuronal cell death in response to amyloid P (AP) exposure in vitro,in animal models of neurodegenerative diseases, and in AD brain itself. Despite this seemingly impressive array of data implicating caspases and apoptosis as etiologic factors in AD, the direct involvement of caspase-dapendent neuronal apoptosis in AD pathogenesis remains uncertain. Alternative explanations for some findings, contradictory experimental observations, and lack of morphologically convincing apoptotic neurons in the vast majority ofAD brains has led to the revised hypothesis that apoptosis-associated molecular events cause neuronal dysfunction in the absence of, or prior to, neuronal death. Unfortunately, this new view renders the term "apoptosis-associated" functionally meaningless since it bears no relationship with apoptotic death and fails to focus scientific investigation on the molecular insults that trigger the "apoptosis-associated" response in AD neurons. On balance, an etiologic role for caspases in AD is far from proven. It remains possible, however, that caspase-dependent neuronal death contributes to AD neuron loss and thus, caspase inhibition offers some hope for extending AD neuron survival so that other agents, targeting upstream events, may delay or reverse primary AD pathology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 15:57:44