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- W3154989265 endingPage "135895" @default.
- W3154989265 startingPage "135895" @default.
- W3154989265 abstract "The disproportionate evolutionary expansion of the human cerebral cortex with reinforcement of cholinergic innervations warranted a major rise in the functional and metabolic load of the conserved basal forebrain (BF) cholinergic system. Given that acetylcholine (ACh) regulates properties of the microtubule-associated protein (MAP) tau and promotes non-amyloidogenic processing of amyloid precursor protein (APP), growing neocortex predicts higher demands for ACh, while the emerging role of BF cholinergic projections in Aβ clearance infers greater exposure of source neurons and their innervation fields to amyloid pathology. The higher exposure of evolutionary most recent cortical areas to the amyloid pathology of Alzheimer’s disease (AD) with synaptic impairments and atrophy, therefore, might involve attenuated homeostatic effects of BF cholinergic projections, in addition to fall-outs of inherent processes of expanding association areas. This unifying model, thus, views amyloid pathology and loss of cholinergic cells as a quid pro quo of the allometric evolution of the human brain, which in combination with increase in life expectancy overwhelm the fine homeostatic balance and set off the disease process." @default.
- W3154989265 created "2021-04-26" @default.
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- W3154989265 creator A5036467116 @default.
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- W3154989265 creator A5075317805 @default.
- W3154989265 date "2021-06-01" @default.
- W3154989265 modified "2023-10-16" @default.
- W3154989265 title "Integrated phylogeny of the human brain and pathobiology of Alzheimer’s disease: A unifying hypothesis" @default.
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