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- W2061313710 abstract "Compelling preclinical and clinical evidence supports a pathophysiological connection between Alzheimer's disease (AD) and diabetes. Altered metabolism, inflammation, and insulin resistance are key pathological features of both diseases. For many years, it was generally considered that the brain was insensitive to insulin, but it is now accepted that this hormone has central neuromodulatory functions, including roles in learning and memory, that are impaired in AD. However, until recently, the molecular mechanisms accounting for brain insulin resistance in AD have remained elusive. Here, we review recent evidence that sheds light on how brain insulin dysfunction is initiated at a molecular level and why abnormal insulin signaling culminates in synaptic failure and memory decline. We also discuss the cellular basis underlying the beneficial effects of stimulation of brain insulin signaling on cognition. Discoveries summarized here provide pathophysiological background for identification of novel molecular targets and for development of alternative therapeutic approaches in AD." @default.
- W2061313710 created "2016-06-24" @default.
- W2061313710 creator A5032823810 @default.
- W2061313710 creator A5040130968 @default.
- W2061313710 creator A5070851422 @default.
- W2061313710 date "2014-02-01" @default.
- W2061313710 modified "2023-10-15" @default.
- W2061313710 title "How does brain insulin resistance develop in Alzheimer's disease?" @default.
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- W2061313710 doi "https://doi.org/10.1016/j.jalz.2013.12.004" @default.
- W2061313710 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24529521" @default.
- W2061313710 hasPublicationYear "2014" @default.
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