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- W2994734275 abstract "Abstract Alzheimer’s disease (AD) is characterised by Aβ and tau pathology as well as synaptic degeneration. Recently, it was suggested that the development of these key disease features may at least in part be due to increased protein synthesis that is regulated by fragile X mental retardation protein (FMRP) and its binding partner CYFIP2. Using an unbiased screen, we show that exposure of primary neurons to Aβ increases FMRP-regulated protein synthesis and involves a reduction of CYFIP2 levels. Modelling this CYFIP2 reduction in mice, we find Aβ accumulation, development of pre-tangle tau pathology, gliosis, loss of synapses, and deficits in memory formation with ageing. We conclude that reducing endogenous CYFIP2 expression is sufficient to cause some key features of AD in mice. We therefore propose a central role for CYFIP2 in AD as a modulator of protein synthesis, highlighting a novel direction for therapeutic targeting." @default.
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- W2994734275 date "2019-12-21" @default.
- W2994734275 modified "2023-10-13" @default.
- W2994734275 title "Alzheimer’s disease-related dysregulation of protein synthesis causes key pathological features with ageing" @default.
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- W2994734275 doi "https://doi.org/10.1101/2019.12.20.884783" @default.
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