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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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| Autori principali: | , , , , , |
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| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
American Society for Clinical Investigation
2004
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC529285/ https://ncbi.nlm.nih.gov/pubmed/15578094 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1172/JCI200422831 |
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