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首页> 外文期刊>Annals of Human Genetics >Mini-review: Role of the PI3K/Akt pathway and tyrosine phosphatases in Alzheimer's disease susceptibility
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Mini-review: Role of the PI3K/Akt pathway and tyrosine phosphatases in Alzheimer's disease susceptibility

机译：迷你评价：在阿尔茨海默病疾病易感性中PI3K / AKT途径和酪氨酸磷酸酶的作用

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A variety of findings from in vitro experiments and animal models support the hypothesis that one contribution to pathogenesis in Alzheimer's disease (AD) is enhanced phosphorylation of tau protein, which may be triggered by amyloid beta (A beta) and mediated by impaired activity of the PI3K/Akt signaling pathway. A number of tyrosine phosphatases act to reduce PI3K/Akt activity, and inhibition of tyrosine phosphatases is protective against A beta toxicity in cell cultures and whole animals. Results from analysis of exome sequenced late onset AD cases and controls similarly show that rare coding variants predicted to damage PI3K functioning increase AD risk, whereas those which are predicted to damage genes for tyrosine phosphatase genes are protective. Taken together, these results support the proposition that tyrosine phosphatase antagonists might be trialed as therapeutic agents to protect against the development of AD.
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