Glial decline and loss of homeostatic support rather than inflammation defines cognitive aging

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The preservation of cognitive longevity and arresting the pandemic of senile dementia engulfing the modern world is arguably the major challenge faced by biomedical research in the 21st century. Age is the leading risk factor for neurodegenerative diseases and vascular dementia, and yet there is a clear distinction between physiological and pathological brain aging; the former proceeds with cognitive abilities mainly preserved, whereas the latter is manifested with rapid cognitive decline. The cellular and molecular mechanisms of brain aging remain disputed, with numerous indications for metabolic and signaling alterations (Mattson and Arumugam, 2018).
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