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Titolo:
APP processing and synaptic plasticity in presenilin-1 conditional knockout mice
Autore:
Yu, HK; Saura, CA; Choi, SY; Sun, LD; Yang, XD; Handler, M; Kawarabayashi, T; Younkin, L; Fedeles, B; Wilson, MA; Younkin, S; Kandel, ER; Kirkwood, A; Shen, J;
Indirizzi:
Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA Brigham & Womens Hosp Boston MA USA 02115 eurol Dis, Boston, MA 02115 USA Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 , Program Neurosci, Boston, MA 02115 USA Johns Hopkins Univ, Mind Brain Inst, Baltimore, MD 21218 USA Johns HopkinsUniv Baltimore MD USA 21218 n Inst, Baltimore, MD 21218 USA MIT, Ctr Learning & Memory, Dept Brain & Cognit Sci, Cambridge, MA 02138 USA MIT Cambridge MA USA 02138 pt Brain & Cognit Sci, Cambridge, MA 02138 USA Mayo Clin Jacksonville, Jacksonville, FL 32224 USA Mayo Clin JacksonvilleJacksonville FL USA 32224 cksonville, FL 32224 USA Columbia Univ, Howard Hughes Med Inst, Ctr Neurobiol & Behav, New York, NY10032 USA Columbia Univ New York NY USA 10032 robiol & Behav, New York, NY10032 USA
Titolo Testata:
NEURON
fascicolo: 5, volume: 31, anno: 2001,
pagine: 713 - 726
SICI:
0896-6273(20010913)31:5<713:APASPI>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; FAMILIAL ALZHEIMERS-DISEASE; GAMMA-SECRETASE ACTIVITY; LONG-TERM POTENTIATION; TRANSGENIC MICE; CULTURED-CELLS; NEURONAL DIFFERENTIATION; VESICLE EXOCYTOSIS; C-TERMINUS; IN-VIVO;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Shen, J Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA Brigham & Womens Hosp Boston MA USA 02115 s, Boston, MA 02115 USA
Citazione:
H.K. Yu et al., "APP processing and synaptic plasticity in presenilin-1 conditional knockout mice", NEURON, 31(5), 2001, pp. 713-726

Abstract

We have developed a presenilin-1 (PS1) conditional knockout mouse (cKO), in which PS1 inactivation is restricted to the postnatal forebrain. The PS1 cKO mouse is viable and exhibits no gross abnormalities. The carboxy-terminal fragments of the amyloid precursor protein differentially accumulate in the cerebral cortex of cKO mice, while generation of beta -amyloid peptidesis reduced. Expression of Notch downstream effector genes, Hes1, Hes5, andDII1, is unaffected in the cKO cortex. Although basal synaptic transmission, long-term potentiation, and long-term depression at hippocampal area CA1synapses are normal, the PS1 cKO mice exhibit subtle but significant deficits in long-term spatial memory. These results demonstrate that inactivation of PS1 function in the adult cerebral cortex leads to reduced A beta generation and subtle cognitive deficits without affecting expression of Notch downstream genes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 22:01:56