Evidence map›Paper›PMID 39871348›Full record

ReviewMolecular neurodegeneration2025

Lipidome disruption in Alzheimer's disease brain: detection, pathological mechanisms, and therapeutic implications.

Sijia He, Ziying Xu, Xianlin Han

Abstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

45 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Sijia HeSam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.ORCID 0000-0003-3786-8770
Ziying XuSam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.ORCID 0000-0003-3725-7726
Xianlin HanSam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA. hanx@uthscsa.edu.ORCID 0000-0002-8615-2413

Funding

TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI RANDY STRONG, Adam Salmon · 1995 to 2026
$30.6M
South Texas Alzheimer's Disease Research CenterP30AG066546 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Sudha Seshadri · 2021 to 2026
$24.0M
San Antonio OAIC - Research Education Component (REC)P30AG044271 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Elena Volpi · 2015 to 2026
$14.1M
TRAINING GRANT ON THE BIOLOGY OF AGINGT32AG021890 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Erzsebet Kokovay, JAMES FLOYD NELSON · 2003 to 2026
$11.4M
Identification of a missing key element underlying apoE2 neuroprotection in Alzheimer's disease and the aging brainRF1AG061872 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HAN, XIANLIN, SESHADRI, SUDHA · 2018 to 2018
$3.4M
Sulfatide deficiency: A novel mechanism leading to reactive astrogliosis in aging and Alzheimer’s diseaseRF1AG061729 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HAN, XIANLIN · 2021 to 2021
$1.9M
The role of sulfatide in the development of tauopathy in the context of ADRDR01AG085545 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lizhen Chen, Jeffrey L. Dupree · 2024 to 2026
$1.8M
Sulfatide deficiency: A novel mechanism leading to reactive astrogliosis in aging and Alzheimer’s diseaseR01AG061729 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HAN, XIANLIN · 2024 to 2025
$1.3M
NIA NIH HHS P30 AG013319NIA NIH HHS P30 AG044271NIA NIH HHS P30 AG066546NIA NIH HHS R01 AG061729NIA NIH HHS R01 AG085545NIA NIH HHS RF1 AG061729NIA NIH HHS RF1 AG061872NIA NIH HHS T32 AG021890
6 · The paper itself

Abstract

Alzheimer's disease (AD) is among the most devastating neurodegenerative disorders with limited treatment options. Emerging evidence points to the involvement of lipid dysregulation in the development of AD. Nevertheless, the precise lipidomic landscape and the mechanistic roles of lipids in disease pathology remain poorly understood. This review aims to highlight the significance of lipidomics and lipid-targeting approaches in the diagnosis and treatment of AD. We summarized the connection between lipid dysregulation in the human brain and AD at both genetic and lipid species levels. We briefly introduced lipidomics technologies and discussed potential challenges and areas of future advancements in the lipidomics field for AD research. To elucidate the central role of lipids in converging multiple pathological aspects of AD, we reviewed the current knowledge on the interplay between lipids and major AD features, including amyloid beta, tau, and neuroinflammation. Finally, we assessed the progresses and obstacles in lipid-based therapeutics and proposed potential strategies for leveraging lipidomics in the treatment of AD.

Indexed as

Alzheimer DiseaseBrainLipid MetabolismLipidomicsAnimalsHumansAlzheimer’s diseaseLipid metabolismLipidomeLipidomics

Identifiers

PMID39871348
PMCPMC11773937

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.