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 |
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Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
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