Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain
Autore:
Moechars, D; Dewachter, I; Lorent, K; Reverse, D; Baekelandt, V; Naidu, A; Tesseur, I; Spittaels, K; Van Den Haute, C; Checler, F; Godaux, E; Cordell, B; Van Leuven, F;
Indirizzi:
KatholieketUniv Leuven, Flemish Inst Biotechnol, Ctr Human Genet, Expt Gene Katholieke Univ Leuven Leuven Belgium B-3000 Ctr Human Genet, Expt Gene Scios Inc, Sunnyvale, CA 94086 USA Scios Inc Sunnyvale CA USA 94086Scios Inc, Sunnyvale, CA 94086 USA CNRS, Inst Pharmacol Mol & Cellulaire, UPR411, F-06560 Valbonne, France CNRS Valbonne France F-06560 ellulaire, UPR411, F-06560 Valbonne, France Univ Mons, Neurosci Lab, B-7000 Mons, Belgium Univ Mons Mons Belgium B-7000 v Mons, Neurosci Lab, B-7000 Mons, Belgium
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 10, volume: 274, anno: 1999,
pagine: 6483 - 6492
SICI:
0021-9258(19990305)274:10<6483:EPCITM>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
FAMILIAL ALZHEIMERS-DISEASE; BETA-PROTEIN; NEUROFIBRILLARY TANGLES; SENILE PLAQUES; NEURONAL LOSS; IN-VIVO; MOUSE; DEFICITS; TERMINUS; DEATH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Van Leuven, F KatholieketUniv Leuven, Flemish Inst Biotechnol, Ctr Human Genet, Expt Gene Katholieke Univ Leuven Campus Gasthuisberg ON 06 Leuven Belgium B-3000
Citazione:
D. Moechars et al., "Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain", J BIOL CHEM, 274(10), 1999, pp. 6483-6492

Abstract

Transgenic mice overexpressing different forms of amyloid precursor protein (APP), i.e. wild type or clinical mutants, displayed an essentially comparable early phenotype in terms of behavior, differential glutamatergic responses, deficits in maintenance of long term potentiation, and premature death. The cognitive impairment, demonstrated in F1 hybrids of the different APP transgenic lines, was significantly different from nontransgenic littermates as early as 3 months of age. Biochemical analysis of secreted and membrane-bound APP, C-terminal "stubs," and A beta(40) and A beta(42) peptides in brain indicated that no single intermediate can be responsible for the complex of phenotypic dysfunctions. As expected, the A beta(42) levels were most prominent in APP/London transgenic mice and correlated directly with the formation of amyloid plaques in older mice of this line, Plaques were associated with immunoreactivity for hyperphosphorylated tau, eventually signaling some form of tau pathology. In conclusion, the different APP transgenic mouse lines studied display cognitive deficits and phenotypic traits early in life that dissociated in time from the formation of amyloid plaques and will be good models for both early and late neuropathological and clinical aspects of Alzheimer's disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 08:05:33