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Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease
BACKGROUND: Knock-in (KI) mouse models of Alzheimer’s disease (AD) that endogenously overproduce Aβ without non-physiological overexpression of amyloid precursor protein (APP) provide important insights into the pathogenic mechanisms of AD. Previously, we reported that App(NL-G-F) mice, which harbor...
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| Pubblicato in: | BMC Neurosci |
|---|---|
| Autori principali: | , , , , |
| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
BioMed Central
2019
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC6425634/ https://ncbi.nlm.nih.gov/pubmed/30894120 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1186/s12868-019-0496-6 |
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