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鞘磷脂和神经酰胺:痴呆症的潜在生物标志物?

Sphingomyelins and ceramides: possible biomarkers for dementia?

作者信息

Loft Laura M I, Moseholm Kristine F, Pedersen Karoline K W, Jensen Majken K, Koch Manja, Cronjé Héléne T

机构信息

Department of Public Health, Section of Epidemiology, University of Copenhagen, Copenhagen, Denmark.

Harvard T.H. Chan School of Public Health, Department of Nutrition, Boston, Massachusetts, USA.

出版信息

Curr Opin Lipidol. 2022 Feb 1;33(1):57-67. doi: 10.1097/MOL.0000000000000804.

Abstract

PURPOSE OF REVIEW

Dementia is a public health challenge with no existing cure or early biomarkers. We review the evidence for blood-based measures of sphingomyelins and ceramides as potential novel biomarkers of dementia.

RECENT FINDINGS

In recent years, lipids have been under investigation for their role in neurodegenerative diseases especially dementia and Alzheimer's disease. Increasing evidence from postmortem human brains suggests that alterations in the metabolism of sphingolipids could play a crucial part in dementia. Findings from epidemiological investigations of blood-based sphingomyelins and ceramides have been inconsistent.

SUMMARY

This review focuses on blood-based measures of 10 specific ceramides and sphingomyelins (Cer C16:0, Cer C20:0, Cer C22:0, Cer C24:0, Cer C24:1 and SM C16:0, SM C20:0, SM C22:0, SM C24:0, SM C24:1) in relation to cognition and dementia. On the bais of 15 studies, there was no robust association between ceramide and sphingomyelin levels and prevalent or incident dementia. Cross-sectionally, Cer C16:0 and Cer C24:1 tends to be higher in dementia cases vs. controls.

摘要

综述目的

痴呆是一项公共卫生挑战,目前尚无治愈方法或早期生物标志物。我们综述了基于血液检测鞘磷脂和神经酰胺作为痴呆潜在新型生物标志物的证据。

最新发现

近年来,脂质在神经退行性疾病尤其是痴呆和阿尔茨海默病中的作用受到研究。来自人类尸检大脑的证据越来越多,表明鞘脂代谢改变可能在痴呆中起关键作用。基于血液的鞘磷脂和神经酰胺的流行病学调查结果并不一致。

总结

本综述重点关注与认知和痴呆相关的10种特定神经酰胺和鞘磷脂(神经酰胺C16:0、神经酰胺C20:0、神经酰胺C22:0、神经酰胺C24:0、神经酰胺C24:1以及鞘磷脂C16:0、鞘磷脂C20:0、鞘磷脂C22:0、鞘磷脂C24:0、鞘磷脂C24:1)的血液检测。基于15项研究,神经酰胺和鞘磷脂水平与现患或新发痴呆之间没有强有力的关联。横断面研究显示,与对照组相比,痴呆患者中神经酰胺C16:0和神经酰胺C24:1往往更高。

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