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Titolo:
Detailed characterization of neuroprotection by a rescue factor Humanin against various Alzheimer's disease-relevant insults
Autore:
Hashimoto, Y; Niikura, T; Ito, Y; Sudo, H; Hata, M; Arakawa, E; Abe, Y; Kita, Y; Nishimoto, I;
Indirizzi:
Keio Univ, Sch Med, Dept Pharmacol & Neurosci, Shinjuku Ku, Tokyo 1608582,Japan Keio Univ Tokyo Japan 1608582 Neurosci, Shinjuku Ku, Tokyo 1608582,Japan
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 23, volume: 21, anno: 2001,
pagine: 9235 - 9245
SICI:
0270-6474(200112)21:23<9235:DCONBA>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; DEPENDENT NEUROTROPHIC FACTOR; HIPPOCAMPAL-NEURONS; PC12 CELLS; OXIDATIVE STRESS; BETA-PEPTIDE; APOPTOSIS; MUTATION; DEATH; GENE;
Keywords:
Humanin; neuronal cell death; rescue; Alzheimer's disease; mutant; A beta;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Nishimoto, I Keio Univ, Sch Med, Dept Pharmacol & Neurosci, Shinjuku Ku, Tokyo 1608582,Japan Keio Univ Tokyo Japan 1608582 njuku Ku, Tokyo 1608582,Japan
Citazione:
Y. Hashimoto et al., "Detailed characterization of neuroprotection by a rescue factor Humanin against various Alzheimer's disease-relevant insults", J NEUROSC, 21(23), 2001, pp. 9235-9245

Abstract

novel factor, termed Humanin (HN), antagonizes against neurotoxicity by various types of familial Alzheimer's disease (AD) genes [V642I and K595N/M596L (NL) mutants of amyloid precursor protein (APP), M146L-presenilin (PS) 1, and N141I-PS2] and by A beta1-43 with clear action specificity ineffective on neurotoxicity by polyglutamine repeat Q79 or superoxide dismutase 1 mutants. Here we report that HN can also inhibit neurotoxicity by other AD-relevant insults: other familial AD genes (A617G-APP, L648P-APP, A246E-PS1, L286V-PS1, C410Y-PS1, and H163R-PS1), APP stimulation by anti-APP antibody, and other A beta peptides (A beta1-42 and A beta 25-35). The action specificity was further indicated by the finding that HN could not suppress neurotoxicity by glutamate or prion fragment. Against the AD-relevant insults, essential roles of Cys 8 and Ser(14) were commonly indicated, and the domain from Pro(3) to Pro(19) was responsible for the rescue action of HN, in which seven residues turned out to be essential. We also compared the neuroprotective action of S14G HN (HNG) with that of activity-dependent neurotrophicfactor, IGF-I, or basic FGF for the antagonism against various AD-relevantinsults (V642I-APP, NL-APP, M146L-PS1, N141I-PS2, and A beta1-43). Although all of these factors could abolish neurotoxicity by A beta -43, only HNG could abolish cytotoxicities by all of them. HN and HN derivative peptides may provide a new insight into the study of AD pathophysiology and allow new avenues for the development of therapeutic interventions for various forms of AD.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 09:54:49