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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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Main Authors: Gong, Bing, Vitolo, Ottavio V., Trinchese, Fabrizio, Liu, Shumin, Shelanski, Michael, Arancio, Ottavio
格式: Artigo
語言:Inglês
出版: American Society for Clinical Investigation 2004
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在線閱讀: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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