Evidence map›Paper›PMID 34997690›Full record

ReviewThe FEBS journal2023

Lipid metabolism and Alzheimer's disease: clinical evidence, mechanistic link and therapeutic promise.

Fei Yin

Open access · greenAbstract readReview
In one paragraph

Review in The FEBS journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
257citing papers in PubMed, 1 pooled it
38.0field-weighted citation impact, top 1% of its field
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

257 citing papers in PubMed, 1 synthesis or guideline pooled it, 361 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. ENT1 inhibition links oligodendrocyte lipid metabolism to connectivity in tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. SIEVEseq: unified differential expression, variability, and skewness analyses using RNA-Seq data.DNA research : an international journal for rapid publication of reports on genes and genomes · 2026
    Article
  17. Article
  18. Review
  19. Review
  20. Kinetic Lipidomics: QuantifyingbioRxiv : the preprint server for biology · 2026
    Article

197 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Fei YinCenter for Innovation in Brain Science, University of Arizona Health Sciences, Tucson, AZ, USA.ORCID 0000-0002-5996-2410
University of Arizona · US

Funding

Timing of Menopausal Hormone Therapy across Perimenopause to Menopause Transition: Neuroimmune System in BrainP01AG026572 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Fei Yin · 2006 to 2026
$53.7M
APOE Regulation of Neuron-Astrocyte Metabolic Coupling in Alzheimer's DiseaseRF1AG068175 · NIA · UNIVERSITY OF ARIZONA · PI YIN, FEI · 2021 to 2021
$1.1M
NIA NIH HHS P01 AG026572NIA NIH HHS RF1 AG068175
6 · The paper itself

Abstract

Alzheimer's disease (AD) is an age-associated neurodegenerative disorder with multifactorial etiology, intersecting genetic and environmental risk factors, and a lack of disease-modifying therapeutics. While the abnormal accumulation of lipids was described in the very first report of AD neuropathology, it was not until recent decades that lipid dyshomeostasis became a focus of AD research. Clinically, lipidomic and metabolomic studies have consistently shown alterations in the levels of various lipid classes emerging in early stages of AD brains. Mechanistically, decades of discovery research have revealed multifaceted interactions between lipid metabolism and key AD pathogenic mechanisms including amyloidogenesis, bioenergetic deficit, oxidative stress, neuroinflammation, and myelin degeneration. In the present review, converging evidence defining lipid dyshomeostasis in AD is summarized, followed by discussions on mechanisms by which lipid metabolism contributes to pathogenesis and modifies disease risk. Furthermore, lipid-targeting therapeutic strategies, and the modification of their efficacy by disease stage, ApoE status, and metabolic and vascular profiles, are reviewed.

Indexed as

Alzheimer DiseaseBrainEnergy MetabolismHumansLipid MetabolismOxidative Stressalzheimer’s diseasefatty acidlipid metabolismtherapeutics

Identifiers

PMID34997690
PMCPMC9259766
OpenAlexW4206661596

What Socratic holds

Textmetadata
LicenceTDM
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.