Evidence map›Paper›PMID 39913635›Full record

ArticlePloS one2025

The impact of apolipoprotein E, type ∊4 allele on Alzheimer's disease pathological biomarkers: a comprehensive post-mortem pilot-analysis.

Ziyu Wan, Tao Ma

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

2 authors.

Ziyu WanDepartment of Internal Medicine, Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.ORCID 0009-0009-2443-6435
Tao MaDepartment of Internal Medicine, Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.ORCID 0000-0002-0763-7261

Funding

Targeting protein synthesis dysregulation in Down syndrome-associated cognitive impairment with agingR01AG073823 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Tao Ma · 2021 to 2026
$2.3M
Roles of the glycogen synthase kinase 3 alpha isoform in Alzheimers disease pathophysiologyRF1AG082388 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2023 to 2023
$1.6M
NIA NIH HHS R01 AG073823NIA NIH HHS RF1 AG082388
6 · The paper itself

Abstract

The apolipoprotein E type ∊4 allele (ApoE4) is known as the strongest genetic risk factor for Alzheimer's Disease (AD). Meanwhile, many aspects of its impact on AD pathology remain underexplored. This study conducts a systematic data analysisof donor data from the Seattle Alzheimer's Disease Brain Cell Atlas. Our investigation delves into the intricate interplay between identified biomarkers and their correlation with ApoE4 across all severities of AD. Employing Pearson R correlation, and one-way and two-way ANOVA tests, we elucidate the pathological changes in biomarkers and the altering effects of ApoE4. Remarkably, the phosphorylation of tau observed in neurofibrillary tangles (NFTs) marked by the AT8 antibody, emerges as the most correlated factor with other pathological biomarkers. This correlation is mediated by both tau and amyloid pathology, suggesting a higher hierarchical role in determining AD pathological effects than other biomarkers. However, non-ApoE4 carriers exhibit a more significant correlation with disease progression severity compared to ApoE4 carriers, though ApoE4 carriers demonstrate significance in exacerbating the effect of accumulating phosphorylated tau and amyloid plaques assessed by AT8 and 6E10 antibodies. Furthermore, our analysis does not observe dramatic neuronal changes in grey matter across the span of AD pathology. Glia activation, measured by Iba1 and GFAP, demonstrates an amyloid-specific correlation. This research marks the first human post-mortem analysis providing a comprehensive examination of prevailing AD biomarkers and their interconnectedness with pathology and ApoE4 genetic factor. Limitations in the study are acknowledged, underscoring the need for further exploration and refinement in future research endeavors.

Indexed as

Alzheimer DiseaseApolipoprotein E4AgedAged, 80 and overAllelesAutopsyBiomarkersBrainFemaleHumansMaleNeurofibrillary TanglesPhosphorylationPilot ProjectsPlaque, Amyloidtau ProteinsApolipoprotein E4Biomarkerstau Proteins

Identifiers

PMID39913635
PMCPMC11801730

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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.