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Insulin resistance: an emerging link in Alzheimer's disease.

机译:胰岛素抵抗:阿尔茨海默氏病的新兴联系。

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摘要

Relentless progression of Alzheimer's disease (AD) poses a grave situation for the biomedical community to tackle. Agents starting as hot favorites in clinical trials have failed in later stages and it is time we reconsidered our approaches to intervene the disease. Quite some interesting work in the last decade has introduced a new school of thought which factors in neuronal glycemic imbalance as a major component for the development of AD. Insulin resistance in the brain has brought forward subsequent sequelae which might work towards amyloid accretion and/or tau hyperphosphorylation. It is also pointed out that insulin works by distributing iron to neuronal tissue and an insulin resistant state throws it off gear leading to iron overloading of neurons which is ultimately detrimental. A relatively recent investigation finds the role of c-Jun-N-terminal kinase (JNK3) in AD which also seems to bear a link with insulin resistance.
机译:阿尔茨海默氏病(AD)的持续发展给生物医学界带来了严峻的形势。开始在临床试验中成为热门药物的药物在后来阶段失败了,现在该是我们重新考虑干预疾病的方法了。在过去十年中,许多有趣的工作引入了一种新的思想流派,其将神经元血糖失衡因素作为AD发展的主要组成部分。大脑中的胰岛素抗性带来了后续的后遗症,可能有助于淀粉样蛋白的积聚和/或tau过度磷酸化。还指出,胰岛素通过将铁分布到神经元组织而起作用,并且胰岛素抵抗状态使它失去作用,导致神经元铁超载,这最终是有害的。一项相对较新的研究发现c-Jun-N-末端激酶(JNK3)在AD中的作用似乎也与胰岛素抵抗有关。

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