Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in...
Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease
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England: BioMed Central
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English
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England: BioMed Central
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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
mice, which harbor three familial AD mutations (Swedish, Beyreuther/Iberian, and Arct...
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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
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TN_cdi_doaj_primary_oai_doaj_org_article_2e4b995e9db14d0fba218203e3134f29
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https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_2e4b995e9db14d0fba218203e3134f29
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ISSN
1471-2202
E-ISSN
1471-2202
DOI
10.1186/s12868-019-0496-6
