STIM2蛋白的高表达降低了阿尔茨海默病小鼠模型大脑中β斑块的数量

IF 0.2 Q4 PHYSICS, MULTIDISCIPLINARY

St Petersburg Polytechnic University Journal-Physics and Mathematics Pub Date : 2016-12-01 DOI:10.1016/j.spjpm.2016.11.009

Daria P. Chernyuk , Olga L. Vlasova , Ilya B. Bezprozvanny , Elena A. Popugaeva

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引用次数: 2

摘要

在同时表达淀粉样蛋白和早老素毒性的阿尔茨海默病(AD) 5FAD小鼠模型中，研究了STIM2→nSOCE信号通路的作用。我们观察到成年5FAD小鼠在4、6月龄时海马中STIM2蛋白表达下调。结果表明，PSD95蛋白和STIM2蛋白的表达均下调。结果表明，成年小鼠海马区高表达STIM2蛋白可使5FAD小鼠皮层淀粉样斑块数量减少3倍。观察到的数据证实了科学假设，即激活stim2依赖性储存操作钙进入可以对治疗AD产生治疗作用。

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Hyperexpression of STIM2 protein lowers the amount of Abeta plaques in the brain of Alzheimer's disease mouse model

The role of the STIM2→nSOCE signaling pathway was investigated in a model of Alzheimer's disease (AD) 5FAD mice that express amyloid and presenilin toxicity simultaneously. It was observed that expression of STIM2 protein was downregulated in the hippocampus of adult 5FAD mice at the age of 4 and 6 months. It was shown that expression of PSD95 protein was downregulated together with STIM2 protein. It was established that hyperexpression of STIM2 protein in the hippocampus of adult mice lowered the amount of amyloid plaques in the cortex of 5FAD mice by three times. The observed data confirms the scientific hypothesis that activation of STIM2-dependent store-operated calcium entry can have a therapeutic effect for treatment in AD.

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来源期刊

St Petersburg Polytechnic University Journal-Physics and Mathematics PHYSICS, MULTIDISCIPLINARY-

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50.00%

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