Evidence map›Paper›PMID 39885546›Full record

ArticleJournal of neuroinflammation2025

APOEε4 alters ApoE and Fabp7 in frontal cortex white matter in prodromal Alzheimer's disease.

Marta Moreno-Rodriguez, Sylvia E Perez, Michael Malek-Ahmadi, Elliott J Mufson

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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

4 authors.

Marta Moreno-RodriguezDepartment of Translational Neuroscience, Barrow Neurological Institute, Phoenix, AZ, 85013, USA.
Sylvia E PerezDepartment of Translational Neuroscience, Barrow Neurological Institute, Phoenix, AZ, 85013, USA.
Michael Malek-AhmadiBanner Alzheimer's Institute, Phoenix, AZ, 85006, USA.
Elliott J MufsonDepartment of Translational Neuroscience, Barrow Neurological Institute, Phoenix, AZ, 85013, USA. elliott.mufson@barrowneuro.org.

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1991 to 2020
$49.1M
TAU, AB, SYNUCLEIN AND NITRATIVE/OXIDATIVE DAMAGE IN MCIP01AG014449 · NIA · UNIVERSITY OF PITTSBURGH · PI MUFSON, ELLIOTT JAY · 1997 to 2024
$39.7M
Rush Alzheimer's Disease Research CenterP30AG072975 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI Lisa L Barnes, Julie A. Schneider · 2021 to 2026
$24.7M
Cellular and Molecular Medial Temporal Lobe Pathology in Elderly PreMCI subjectsR01AG043375 · NIA · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI GINSBERG, STEPHEN D, MUFSON, ELLIOTT JAY · 2013 to 2017
$3.6M
Default mode network dysfunction in Down SyndromeRF1AG081286 · NIA · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI MUFSON, ELLIOTT JAY, PEREZ, SYLVIA EVA · 2023 to 2023
$1.8M
Neuroprotective microRNA pathwaysR21AG042146 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI COUNTS, SCOTT E · 2012 to 2013
$409k
National Institute of Aging P30AG010161National Institute of Aging P30AG042146National Institute of Aging PO1AG014449National Institute of Aging RF1AG081286National Institute of Aging RO1AG043375NIA NIH HHS P01 AG014449NIA NIH HHS P30 AG010161NIA NIH HHS P30 AG072975NIA NIH HHS R01 AG043375NIA NIH HHS R21 AG042146NIA NIH HHS RF1 AG081286
6 · The paper itself

Abstract

The ApoE ε4 allele (APOEε4) is a major genetic risk factor for sporadic Alzheimer's disease (AD) and is linked to demyelination and cognitive decline. However, its effects on the lipid transporters apolipoprotein E (ApoE) and fatty acid-binding protein 7 (Fabp7), which are crucial for the maintenance of myelin in white matter (WM) during the progression of AD remain underexplored. To evaluate the effects of APOEε4 on ApoE, Fabp7 and myelin in the WM of the frontal cortex (FC), we examined individuals carrying one ε4 allele that came to autopsy with a premortem clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment (MCI) and mild to moderate AD compared with non-carrier counterparts. ApoE, Fabp7 and Olig2 immunostaining was used to visualize cells, whereas myelin basic protein (MBP) immunocytochemistry and luxol fast blue (LFB) histochemistry of myelin in the WM of the FC were combined with quantitative morphometry. We observed increased numbers of ApoE-positive astrocytes in the WM of both NCI and MCI APOEε4 carriers compared with non-carriers, whereas Fabp7-positive cells were elevated only in AD. Conversely, Olig2 cell counts and MBP immunostaining decreased in MCI APOEε4 carriers compared to non-carriers, while LFB levels were higher in NCI APOEε4 carriers compared to non-carriers. Although no correlations were found between ApoE, Fabp7, and cognitive status, LFB measurements were positively correlated with perceptual speed, global cognition, and visuospatial scores in APOEε4 carriers across clinical groups. The present findings suggest that the ε4 allele compromises FC myelin homeostasis by disrupting the lipid transporters ApoE, Fabp7 and myelination early in the onset of AD. These data support targeting cellular components related to WM integrity as possible treatments for AD.

Indexed as

Alzheimer DiseaseApolipoproteins EFatty Acid-Binding Protein 7Frontal LobeTumor Suppressor ProteinsWhite MatterAgedAged, 80 and overCognitionDisease ProgressionHumansImmunohistochemistryMalePhosphorylationApoE protein, humanApolipoproteins EFABP7 protein, humanFatty Acid-Binding Protein 7Tumor Suppressor ProteinsAlzheimer's diseaseAPOEε4AstrocytesFabp7Mild cognitive impairmentWhite matter

Identifiers

PMID39885546
PMCPMC11783964

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Registered trials

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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 OpenQuestion graph.