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对施密特等人的回应:胆固醇酯转移蛋白(CETP)活性降低与痴呆风险:一项孟德尔随机化分析

Response to Schmidt et al.: Lower activity of cholesteryl ester transfer protein (CETP) and the risk of dementia: a Mendelian randomization analysis.

作者信息

Anderson Emma L

机构信息

Division of Psychiatry, University College London, 149 Tottenham Court Road, W1T 7NF, London, UK.

出版信息

Alzheimers Res Ther. 2024 Dec 19;16(1):264. doi: 10.1186/s13195-024-01631-4.

Abstract

A recent paper concluded that cholesteryl ester transfer protein (CETP) inhibition may be a viable target to treat dementia, based on human genetic evidence of a protective effect of target inhibition on risk of Lewy body and Parkinson's dementia. Alzheimer's disease, which is by far the most prevalent cause of dementia (around 80% of all dementia cases) was not included as an outcome. Evidence shows CETP inhibition is unlikely to affect Alzheimer's risk and may even potentially modestly increase risk. There is also little evidence to support an effect of CETP inhibition on all-cause or vascular dementia. Thus, CETP inhibition is unlikely to be a viable target to treat the most prevalent causes of dementia.

摘要

最近一篇论文得出结论,基于对靶标抑制对路易体痴呆和帕金森痴呆风险具有保护作用的人类遗传学证据,胆固醇酯转运蛋白(CETP)抑制可能是治疗痴呆的一个可行靶点。但作为研究结果,最常见的痴呆病因——阿尔茨海默病(约占所有痴呆病例的80%)未被纳入。有证据表明,CETP抑制不太可能影响患阿尔茨海默病的风险,甚至可能会适度增加风险。也几乎没有证据支持CETP抑制对全因性痴呆或血管性痴呆有影响。因此,CETP抑制不太可能成为治疗最常见痴呆病因的可行靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f72/11660916/fc9d127f6a30/13195_2024_1631_Fig1_HTML.jpg

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