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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Vydáno v:BMC Neurosci
Hlavní autoři: Sakakibara, Yasufumi, Sekiya, Michiko, Saito, Takashi, Saido, Takaomi C., Iijima, Koichi M.
Médium: Artigo
Jazyk:Inglês
Vydáno: BioMed Central 2019
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Research Article
On-line přístup: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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