期刊
NEUROCHEMICAL RESEARCH
卷 45, 期 7, 页码 1481-1491出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-020-03031-0
关键词
Alzheimer's disease; Hypometaboilsm; Type 2 diabetes; Type 3 diabetes insulin; Glucose
Recent studies continue to find evidence linking Type 2 diabetes (T2D) with Alzheimer's disease (AD), the most common cause of dementia, a general term for memory loss and other cognitive abilities serious enough to interfere with daily life. Insulin resistance or dysfunction of insulin signaling is a universal feature of T2D, the main culprit for altered glucose metabolism and its interdependence on cell death pathways, forming the basis of linking T2D with AD as it may exacerbate A beta accumulation, tau hyperphosphorylation and devastates glucose transportation, energy metabolism, hippocampal framework and promulgate inflammatory pathways. The current work demonstrates the basic mechanisms of the insulin resistance mediates dysregulation of bioenergetics and progress to AD as a mechanistic link between diabetes mellitus and AD. This work also aimed to provide a potential and feasible zone to succeed in the development of therapies in AD by enhanced hypometabolism and altered insulin signaling.
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