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Titolo:
Behavioral disturbances without amyloid deposits in mice overexpressing human amyloid precursor protein with Flemish (A692G) or Dutch (E693Q) mutation
Autore:
Kumar-Singh, S; Dewachter, I; Moechars, D; Lubke, U; De Jonghe, C; Ceuterick, C; Checler, F; Naidu, A; Cordell, B; Cras, P; Van Broeckhoven, C; Van Leuven, F;
Indirizzi:
Univ Antwerp, Flanders Interuniv Inst Biotechnol, Born Bunge Fdn, Dept Biochem, B-2020 Antwerp, Belgium Univ Antwerp Antwerp Belgium B-2020 ept Biochem, B-2020 Antwerp, Belgium Univ Antwerp, Dept Med, Born Bunge Fdn, Neurobiol Lab, B-2020 Antwerp, Belgium Univ Antwerp Antwerp Belgium B-2020 urobiol Lab, B-2020 Antwerp, Belgium Univ Antwerp, Dept Med, Born Bunge Fdn, Lab Electronmicroscopy, B-2020 Antwerp, Belgium Univ Antwerp Antwerp Belgium B-2020 nmicroscopy, B-2020 Antwerp, Belgium Katholieke Univ Leuven, Flanders Interuniv Inst Biotechnol, Ctr Human Genet, Expt Genet Grp, B-3000 Louvain, Belgium Katholieke Univ Leuven LouvainBelgium B-3000 p, B-3000 Louvain, Belgium Janssen Res Fdn, Dept Funct Genomics, B-2340 Beerse, Belgium Janssen Res Fdn Beerse Belgium B-2340 t Genomics, B-2340 Beerse, Belgium CNRS, Inst Pharmacol Mol & Cellulaire, F-06560 Valbonne, France CNRS Valbonne France F-06560 Mol & Cellulaire, F-06560 Valbonne, France Scios Nova Inc, Sunnyvale, CA 94086 USA Scios Nova Inc Sunnyvale CA USA 94086 s Nova Inc, Sunnyvale, CA 94086 USA
Titolo Testata:
NEUROBIOLOGY OF DISEASE
fascicolo: 1, volume: 7, anno: 2000,
pagine: 9 - 22
SICI:
0969-9961(200002)7:1<9:BDWADI>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
FAMILIAL ALZHEIMERS-DISEASE; HEREDITARY CEREBRAL-HEMORRHAGE; TRANSGENIC MOUSE-BRAIN; METHYL-D-ASPARTATE; BETA-PROTEIN; ANIMAL-MODELS; CNS DISORDER; GENE; ANGIOPATHY; DEMENTIA;
Keywords:
Alzheimer's disease; transgenic mice; amyloid precursor protein; Flemish APP mutation; Dutch APP mutation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Kumar-Singh, S Univ Antwerp, Flanders Interuniv Inst Biotechnol, Born Bunge Fdn, Dept Biochem, B-2020 Antwerp, Belgium Univ Antwerp Antwerp BelgiumB-2020 2020 Antwerp, Belgium
Citazione:
S. Kumar-Singh et al., "Behavioral disturbances without amyloid deposits in mice overexpressing human amyloid precursor protein with Flemish (A692G) or Dutch (E693Q) mutation", NEUROBIOL D, 7(1), 2000, pp. 9-22

Abstract

The contribution of mutations in the amyloid precursor protein (APP) gene known as Flemish (APP/A692G) and Dutch (APP/E693Q) to the pathogenesis of Alzheimer's disease and hereditary cerebral hemorrhage with amyloidosis of the Dutch type, respectively, was studied in transgenic mice that overexpress the mutant APP in brain. These transgenic mice showed the same early behavioral disturbances and defects and increased premature death as the APP/London (APP V7171), APP/ Swedish (K670N, M671L), and other APP transgenic mice described previously. Pathological changes included intense glial reaction, extensive microspongiosis in the white matter, and apoptotic neurons in select areas of the brain, while amyloid deposits were absent, even in miceover 18 months of age. This contrasts with extensive amyloid deposition inAPP/London transgenic mice and less pronounced amyloid deposition in APP/Swedish transgenic mice generated identically. It demonstrated, however, that the behavioral deficiencies and the pathological changes in brain resulting from an impaired neuronal function are caused directly by APP or its proteolytic derivative(s). These accelerate or impinge on the normal process of aging and amyloid deposits per se are not essential for this phenotype. (C) 2000 Academic Press.

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Documento generato il 06/04/20 alle ore 21:43:44