Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment

Evidence suggests that Alzheimer disease (AD) begins as a disorder of synaptic function, caused in part by increased levels of amyloid β-peptide 1–42 (Aβ42). Both synaptic and cognitive deficits are reproduced in mice double transgenic for amyloid precursor protein (AA substitution K670N,M671L) and...

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Veröffentlicht in:The Journal of clinical investigation 2004-12, Vol.114 (11), p.1624-1634
Hauptverfasser: Gong, Bing, Vitolo, Ottavio V., Trinchese, Fabrizio, Liu, Shumin, Shelanski, Michael, Arancio, Ottavio
Format: Artikel
Sprache:eng
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