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- W2044904524 endingPage "692" @default.
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- W2044904524 abstract "Alzheimer's disease (AD) is an incurable age-related neurodegenerative disorder characterized by profound memory dysfunction. This bellwether symptom suggests involvement of the hippocampus -- a brain region responsible for memory formation -- and coincidentally an area heavily burdened by hyperphosphorylated tau and neuritic plaques of amyloid beta (Aβ). Recent evidence suggests that pre-fibrillar soluble Aβ underlies an early, progressive loss of synapses that is a hallmark of AD. One of the downstream effects of soluble Aβ aggregates is the activation of the phosphatase calcineurin (CaN). This review details the evidence of CaN hyperactivity in 'normal' aging, models of AD, and actual disease pathogenesis; elaborates on how this could manifest as memory impairment, neuroinflammation, hyperphosphorylated tau, and neuronal death." @default.
- W2044904524 created "2016-06-24" @default.
- W2044904524 creator A5010476718 @default.
- W2044904524 creator A5067568237 @default.
- W2044904524 date "2011-12-01" @default.
- W2044904524 modified "2023-10-02" @default.
- W2044904524 title "A Role for Calcineurin in Alzheimers Disease" @default.
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- W2044904524 doi "https://doi.org/10.2174/157015911798376316" @default.
- W2044904524 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3263462" @default.
- W2044904524 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22654726" @default.
- W2044904524 hasPublicationYear "2011" @default.
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