Evidence map›Paper›PMID 40034502›Full record

ArticleJournal of Alzheimer's disease reports

The causal role of lipids in dementia: A Mendelian randomization study.

Boyang Su, Zhengqing He, Li Mao, Xusheng Huang

Abstract read
In one paragraph

Article in Journal of Alzheimer's disease reports. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

4 authors.

Boyang SuMedical School of Chinese PLA, Beijing, China.
Zhengqing HeDepartment of Neurology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Li MaoNeurological Department of the First Medical Center, Chinese PLA General Hospital, Beijing, China.
Xusheng HuangMedical School of Chinese PLA, Beijing, China.ORCID https://orcid.org/0000-0002-2451-0254

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Increasing evidence suggests that abnormal lipid metabolism is one of the pathogeneses of dementia. It is necessary to reveal the relationship between lipids and dementia. Objective: This study used bidirectional two-sample Mendelian randomization to explore the causal relationship between 179 lipid species and the risk of dementia. Methods: We assessed the causal effects of 179 lipid species and four subtypes of dementia including Alzheimer's disease (AD), vascular dementia (VaD), frontotemporal dementia (FTD), and dementia with Lewy bodies (DLB). Inverse variance weighting, MR-Egger method, weighted median, simple mode, and weighted mode were used to analyze the relationship between lipids and dementia. Cochran's Q, MR-Egger intercept test, and MR-PRESSO test were used to test the heterogeneity and pleiotropy of the results. In addition, we performed an inverse MR analysis testing the causal effects of dementia on lipids. Results: Our study revealed causal effects of glycerophospholipid, glycerolipid, and sterol on the risk of dementia. Phosphatidylcholine, phosphatidylinositol, and triglycerides play significant roles in AD. Notably, phosphatidylcholine played a protective role in both FTD and DLB. However, this study did not observe a significant effect of phosphatidylinositol on FTD. In the case of VaD, not only glycerophospholipid, but also glycerolipid, exerted an influence, but sterol was also a risk factor. Conclusions: Our study provided new evidence supporting the causal role of genetically predicted lipid species in dementia. Future clinical trials are necessary to evaluate the potential role of lipid levels in dementia prevention.

Indexed as

Alzheimer's diseasedementiainstrumental variableslipidsliposomesMendelian randomization

Identifiers

PMID40034502
PMCPMC11864250

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