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Nitric Oxide Signaling Is Recruited As a Compensatory Mechanism for Sustaining Synaptic Plasticity in Alzheimer's Disease Mice
Synaptic plasticity deficits are increasingly recognized as causing the memory impairments which define Alzheimer's disease (AD). In AD mouse models, evidence of abnormal synaptic function is present before the onset of cognitive deficits, and presents as increased synaptic depression revealed...
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| Publicado no: | J Neurosci |
|---|---|
| Main Authors: | , , , , |
| Formato: | Artigo |
| Idioma: | Inglês |
| Publicado em: |
Society for Neuroscience
2015
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| Assuntos: | |
| Acesso em linha: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4412902/ https://ncbi.nlm.nih.gov/pubmed/25926464 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1523/JNEUROSCI.4002-14.2015 |
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