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Titolo:
Hypothesis: amyloid beta-peptides truncated at the N-terminus contribute to the pathogenesis of Alzheimer's disease
Autore:
Larner, AJ;
Indirizzi:
Natl Hosp Neurol & Neurosurg, London WC1N 3BG, England Natl Hosp Neurol & Neurosurg London England WC1N 3BG n WC1N 3BG, England
Titolo Testata:
NEUROBIOLOGY OF AGING
fascicolo: 1, volume: 20, anno: 1999,
pagine: 65 - 69
SICI:
0197-4580(199901/02)20:1<65:HABTAT>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
PRECURSOR PROTEIN; APOLIPOPROTEIN-E; SENILE PLAQUES; IN-VITRO; CORE PROTEIN; DEPOSITION; BRAIN; PATHOLOGY; FRAGMENT; P3;
Keywords:
Alzheimer's disease; amyloid beta-peptides; fragments; neurotoxicity; pathogenesis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Larner, AJ Natl Hosp Neurol & Neurosurg, Queen Sq, London WC1N 3BG, England Natl Hosp Neurol & Neurosurg Queen Sq London England WC1N 3BG
Citazione:
A.J. Larner, "Hypothesis: amyloid beta-peptides truncated at the N-terminus contribute to the pathogenesis of Alzheimer's disease", NEUROBIOL A, 20(1), 1999, pp. 65-69

Abstract

Fragments of amyloid beta-peptide truncated at the N-terminus are present in AD brain early in the course of Alzheimer's disease. It is proposed thatthese species contribute to the pathogenesis of AD, possibly through destabilization of elements of the neuronal cytoskeleton by small fibrillar deposits. (C) 1999 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 13:29:07