Evidence map›Paper›PMID 36429044›Full record

ArticleCells2022

Lipid Dys-Homeostasis Contributes to APOE4-Associated AD Pathology.

Adina-Nicoleta Lazar, Linda Hanbouch, Lydie Boussicaut, Baptiste Fourmaux, Patricia Daira, Mark J Millan, Nathalie Bernoud-Hubac, Marie-Claude Potier

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Alzheimer's Disease: A Suitable Case for Treatment with Precision Medicine?Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2024
    Review
  9. Review
  10. Review
  11. Effect of choline supplementation in presymptomaticAlzheimer's & dementia (New York, N. Y.)
    Article
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

8 authors at 3 institutions in 2 countries.

Adina-Nicoleta LazarUniv Lyon, INSA Lyon, CNRS, LaMCoS, UMR5259, 69621 Villeurbanne, France.
Linda HanbouchICM Paris Brain Institute, CNRS UMR7225, INSERM U1127, Sorbonne University, Hôpital de la Pitié-Salpêtrière, 47 Bd de l'Hôpital, 75013 Paris, France.
Lydie BoussicautICM Paris Brain Institute, CNRS UMR7225, INSERM U1127, Sorbonne University, Hôpital de la Pitié-Salpêtrière, 47 Bd de l'Hôpital, 75013 Paris, France.
Baptiste FourmauxUniv Lyon, INSA Lyon, CNRS, LaMCoS, UMR5259, 69621 Villeurbanne, France.
Patricia DairaUniv Lyon, INSA Lyon, CNRS, LaMCoS, UMR5259, 69621 Villeurbanne, France.
Mark J MillanInstitut De Recherche Servier IDRS, Neuroscience Inflammation Thérapeutic Area, 125 Chemin de Ronde, 78290 Croissy-sur-Seine, France.
Nathalie Bernoud-HubacUniv Lyon, INSA Lyon, CNRS, LaMCoS, UMR5259, 69621 Villeurbanne, France.ORCID 0000-0001-8009-5983
Marie-Claude PotierICM Paris Brain Institute, CNRS UMR7225, INSERM U1127, Sorbonne University, Hôpital de la Pitié-Salpêtrière, 47 Bd de l'Hôpital, 75013 Paris, France.ORCID 0000-0003-2462-7150
Université Claude Bernard Lyon 1 · FRCentre National de la Recherche Scientifique · FRServier (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The association of the APOE4 (vs. APOE3) isoform with an increased risk of Alzheimer's disease (AD) is unequivocal, but the underlying mechanisms remain incompletely elucidated. A prevailing hypothesis incriminates the impaired ability of APOE4 to clear neurotoxic amyloid-β peptides (Aβ) from the brain as the main mechanism linking the apolipoprotein isoform to disease etiology. The APOE protein mediates lipid transport both within the brain and from the brain to the periphery, suggesting that lipids may be potential co-factors in APOE4-associated physiopathology. The present study reveals several changes in the pathways of lipid homeostasis in the brains of mice expressing the human APOE4 vs. APOE3 isoform. Carriers of APOE4 had altered cholesterol turnover, an imbalance in the ratio of specific classes of phospholipids, lower levels of phosphatidylethanolamines bearing polyunsaturated fatty acids and an overall elevation in levels of monounsaturated fatty acids. These modifications in lipid homeostasis were related to increased production of Aβ peptides as well as augmented levels of tau and phosphorylated tau in primary neuronal cultures. This suite of APOE4-associated anomalies in lipid homeostasis and neurotoxic protein levels may be related to the accrued risk for AD in APOE4 carriers and provides novel insights into potential strategies for therapeutic intervention.

Indexed as

Alzheimer DiseaseApolipoprotein E4AnimalsApolipoprotein E3Apolipoproteins EHomeostasisHumansMiceProtein IsoformsApolipoprotein E3Apolipoprotein E4Apolipoproteins EProtein IsoformsAlzheimer’s diseaseAPOE4Aβ peptidelipid homeostasistau

Identifiers

PMID36429044
PMCPMC9688773
OpenAlexW4309314170

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.