The Novel Implication of Androgen in Diabetes-induced Alzheimer’s Disease
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Alzheimer’s disease (AD) is characterized by the accumulation of amyloid beta (Aβ) and the hyperphosphorylation of tauprotein in the brain, leading to the increase in inflammation and neuronal loss. Recently, evidences to support the associationbetween type 2 diabetes mellitus (T2DM) and AD have markedly increased by clinical researches and experimental studies. Reduced insulin action and impaired glucose metabolism in the brain leads to diabetes induced AD. Androgen, a malesex hormone, was known to regulate inflammatory response, Aβ deposition in AD, insulin signaling, and synaptic plasticityin brain. Clinical studies demonstrated that androgen deficiency results in the increased risk of AD and its severe progressionin male subjects. We reviewed the significant evidences to support that low testosterone levels are linked to diabetes-inducedAD based on previous studies. Thus, we highlight the therapeutic potential of androgen in diabetes induced AD. (J LipidAtheroscler 2017 December;6(2):66-74)
Abstract
Alzheimer’s disease (AD) is characterized by the accumulation of amyloid beta (Aβ) and the hyperphosphorylation of tauprotein in the brain, leading to the increase in inflammation and neuronal loss. Recently, evidences to support the associationbetween type 2 diabetes mellitus (T2DM) and AD have markedly increased by clinical researches and experimental studies. Reduced insulin action and impaired glucose metabolism in the brain leads to diabetes induced AD. Androgen, a malesex hormone, was known to regulate inflammatory response, Aβ deposition in AD, insulin signaling, and synaptic plasticityin brain. Clinical studies demonstrated that androgen deficiency results in the increased risk of AD and its severe progressionin male subjects. We reviewed the significant evidences to support that low testosterone levels are linked to diabetes-inducedAD based on previous studies. Thus, we highlight the therapeutic potential of androgen in diabetes induced AD. (J LipidAtheroscler 2017 December;6(2):66-74)
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