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Titolo:
Caspases and neurodegeneration: on the cutting edge of new therapeutic approaches
Autore:
Wellington, CL; Hayden, MR;
Indirizzi:
Univ British Columbia, Ctr Mol Med & Therapeut, Womens & Childrens Hosp, Vancouver, BC, Canada Univ British Columbia Vancouver BC Canada ns Hosp, Vancouver, BC, Canada
Titolo Testata:
CLINICAL GENETICS
fascicolo: 1, volume: 57, anno: 2000,
pagine: 1 - 10
SICI:
0009-9163(200001)57:1<1:CANOTC>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; DISEASE ASSOCIATED PRESENILIN-1; HUNTINGTONS-DISEASE; POLYGLUTAMINE TRACT; COMBINATORIAL APPROACH; TERMINAL FRAGMENTS; REPEAT LENGTH; BETA-PROTEIN; CAG REPEAT; IN-VIVO;
Keywords:
caspases; neurodegeneration; therapeutic approaches;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Hayden, MR Ctr Mol Med & Therapeut, 980 W 28th Ave, Vancouver, BC V5Z 4H4,Canada Ctr Mol Med & Therapeut 980 W 28th Ave Vancouver BC Canada V5Z 4H4
Citazione:
C.L. Wellington e M.R. Hayden, "Caspases and neurodegeneration: on the cutting edge of new therapeutic approaches", CLIN GENET, 57(1), 2000, pp. 1-10

Abstract

Unregulated apoptosis underlies many pathological conditions, including neurodegenerative diseases. In this review, we focus on the role of cysteine aspartate-specific proteases (caspase) activity in Huntington disease (HD) and Alzheimer disease (AD) as two representative neurodegenerative disorders that normally manifest in mid- to late-life. Caspases appear to be involved in the molecular pathology of HD by directly cleaving huntingtin and generating toxic protein fragments containing the polyglutamine tract, and by being recruited and activated by polyglutamine-containing aggregates composed mainly of truncated huntingtin fragments. Several proteins involved in AD, including beta-amyloid precursor protein (APP) and presenilins (PSs), are also cleaved by caspases. For APP, caspase cleavage may contribute to toxicity by generating toxic fragments or by shifting APP processing toward anamyloidogenic pathway. For PSs, caspase cleavage disables antiapoptotic functions attributed to PS C-terminal fragments. These observations suggest that caspases actively contribute to the molecular pathogenesis of these diseases and support the development of caspase inhibitors as potential therapeutic approaches for chronic neurodegenerative disorders.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 10:11:31