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Titolo:
Alzheimer disease - Mouse models pave the way for therapeutic opportunities
Autore:
Emilien, G; Maloteaux, JM; Beyreuther, K; Masters, CL;
Indirizzi:
Catholic Univ Louvain, Clin Univ St Luc, Pharmacol Lab, Brussels, Belgium Catholic Univ Louvain Brussels Belgium Pharmacol Lab, Brussels, Belgium Catholic Univ Louvain, Clin Univ St Luc, Dept Neurol, Brussels, Belgium Catholic Univ Louvain Brussels Belgium , Dept Neurol, Brussels, Belgium Univ Heidelberg, Zentrum Mol Biol, D-6900 Heidelberg, Germany Univ Heidelberg Heidelberg Germany D-6900 ol, D-6900 Heidelberg, Germany Univ Melbourne, Dept Pathol, Parkville, Vic 3052, Australia Univ Melbourne Parkville Vic Australia 3052 arkville, Vic 3052, Australia Mental Hlth Res Inst, Parkville, Vic 3052, Australia Mental Hlth Res InstParkville Vic Australia 3052 le, Vic 3052, Australia
Titolo Testata:
ARCHIVES OF NEUROLOGY
fascicolo: 2, volume: 57, anno: 2000,
pagine: 176 - 181
SICI:
0003-9942(200002)57:2<176:AD-MMP>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; TRANSGENIC MICE; APOLIPOPROTEIN-E; MUTANT PRESENILIN-1; BETA-PEPTIDE; DEPOSITION; MUTATIONS; MISSENSE; PLAQUES; BRAINS;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Emilien, G 127 Rue Henri Prou, F-78340 Les Clayes Bois, France 127 Rue Henri Prou Les Clayes Bois France F-78340 ois, France
Citazione:
G. Emilien et al., "Alzheimer disease - Mouse models pave the way for therapeutic opportunities", ARCH NEUROL, 57(2), 2000, pp. 176-181

Abstract

Research into the molecular mechanisms of Alzheimer disease (AD) continuesto clarify important issues in aberrant protein processing while seeking to identify therapeutic targets. Mutations of genes on chromosomes I, lif (presenilins 1 and 2), and 21 (the amyloid-beta [A beta] amyloid precursor protein [APP]) cause the familial forms of AD that often begin before age 65. An allelic polymorphism on chromosome 19 (apolipoprotein E) affects the age of onset of the more common forms of sporadic AD. Multiple studies in transgenic mice provide strong evidence to support the view that A beta amyloid formation is an early and critical pathogenic event: mice expressing pathogenic human APP mutations develop A beta deposits; coexpression of mutant presenilin genes accelerates the rate of A beta deposition; and apolipoprotein E plays a role in this process. Thus, the 3 established genetic causes or risk factors for AD affect A beta deposition. The fact that elevation ofthe A beta 42/A beta 40 ratio (differing only in 2 amino acids in length) is also linked to amyloid deposition in the APP mice and is temporally linked to cognitive impairment suggests that A beta 42 may be a principal inducing factor of AD. The exact sequence of events is still unknown, but the transgenic models generated so far have shown their usefulness in clarifying this complex part of the pathology, The continuing progress in elucidation of the molecular pathogenesis of AD suggests a range of rational pharmacological interventions for this disorder. The most promising strategy involvesthe development of approaches to retard, halt, or prevent A beta-mediated disease progression, and these can now be tested in transgenic animals.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 18:33:44