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Titolo:
SYNAPTIC BETA-AMYLOID PRECURSOR PROTEINS INCREASE WITH LEARNING-CAPACITY IN RATS
Autore:
HUBER G; BAILLY Y; MARTIN JR; MARIANI J; BRUGG B;
Indirizzi:
F HOFFMANN LA ROCHE & CO LTD,PRECLIN CNS RES,DIV PHARMA CH-4002 BASELSWITZERLAND CNRS,LAB NEUROBIOL CELLULAIRE STRASBOURG FRANCE UNIV PARIS 06,INST NEUROSCI,CNRS PARIS FRANCE
Titolo Testata:
Neuroscience
fascicolo: 2, volume: 80, anno: 1997,
pagine: 313 - 320
SICI:
0306-4522(1997)80:2<313:SBPPIW>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALZHEIMERS-DISEASE; NEURITE OUTGROWTH; CORTICAL-NEURONS; AXONAL-TRANSPORT; IN-VIVO; BRAIN; MICE; LOCALIZATION; INHIBITORS; EXPRESSION;
Keywords:
BETA-AMYLOID PRECURSOR PROTEINS; BEHAVIOR; COGNITION; SYNAPSE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
G. Huber et al., "SYNAPTIC BETA-AMYLOID PRECURSOR PROTEINS INCREASE WITH LEARNING-CAPACITY IN RATS", Neuroscience, 80(2), 1997, pp. 313-320

Abstract

The precursor proteins of Alzheimer's disease beta-amyloid peptide, the beta-amyloid precursor protein isoforms, comprise a family of neuronal proteins with synaptic localization whose physiological roles in brain are poorly understood. One possible role for synaptic proteins isinvolvement in neuronal plasticity. After exposure to an enriched environment compared to impoverished conditions, rats exhibited superior cognitive capacity. Up to similar to four-fold increased overall levels of beta-amyloid precursor proteins were found in cortical/subcortical tissue of the enriched animals displaying significantly more synapses immunoreactive for the different beta-amyloid precursor protein isoforms (beta-amyloid precursor protein(695)- and beta-amyloid precursor protein(751,770)) in hippocampus and adjacent occipital cortex. This correlation thus provides in vivo evidence for an association of beta-amyloid precursor proteins with plastic changes induced by complex environment with consequences for cognitive functions and suggests that impaired beta-amyloid precursor protein metabolism at synapses might contribute to brain dysfunction in Alzheimer's disease. (C) 1997 IBRO. Published by Elsevier Science Ltd.

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Documento generato il 02/07/20 alle ore 21:35:52