Evidence mapPaperPMID 41388809Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025

APOE isoform-associated tau oligomer polymorphs differ in synaptotoxicity and seeding activity.

Naomi Moreno, Nikita Shchankin, Leiana Fung, Nicha Puangmalai, Nemil Bhatt, Md Anzarul Haque, Yingxin Zhao, C Dirk Keene, Agenor Limon, Rakez Kayed

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 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. APOE isoform-associated tau oligomer polymorphs differ in synaptotoxicity and seeding activity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    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

10 authors.

Naomi MorenoMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, Texas, USA.ORCID 0000-0003-0482-1394
Nikita ShchankinMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, Texas, USA.
Leiana FungMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, Texas, USA.
Nicha PuangmalaiMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, Texas, USA.
Nemil BhattMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, Texas, USA.
Md Anzarul HaqueMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, Texas, USA.
Yingxin ZhaoSealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston, Texas, USA.
C Dirk KeeneDivision of Neuropathology, University of Washington, Seattle, Washington, USA.
Agenor LimonMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, Texas, USA.
Rakez KayedMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, Texas, USA.

Funding

University of Washington Alzheimer's Disease Research CenterP30AG066509 · NIA · UNIVERSITY OF WASHINGTON · PI Caitlin Shannon Latimer · 2020 to 2026
$29.0M
NIA NIH HHS P30 AG066509NIH HHS AG05402506NIH HHS AG06071801NIH HHS AG067952NIH HHS AG070255NIH HHS AG07245801NIH HHS AG073133NIH HHS AG07725301NIH HHS AG077484
6 · The paper itself

Abstract

introductionPathological tau aggregates form distinct polymorphic species across diseases and even across Alzheimer's disease (AD) patients. However, tau aggregate polymorphism across the apolipoprotein E isoforms (APOE ε2, ε3, ε4), the strongest predictors of late-onset AD development, is unknown.

methodsThis study assessed the conformational and bioactivity properties of tau oligomers from 14 patients with varying APOE genotypes.

resultsTau oligomers differ in proteolytic stability and cleavage site profiles across the APOE isoforms, indicating conformationally distinct polymorphs. APOE isoform-associated tau oligomers affect synaptic plasticity differently, with ε4-associated oligomers having the highest potency and strongest impact on synaptic functioning. Bioactivity assays reveal that ε4-associated oligomers demonstrate particularly high seeding activity. Interestingly, tau oligomer synaptotoxicity and seeding activity are independent characteristics. DISCUSSION: The APOE isoforms are associated with distinct tau oligomer polymorphs with varying bioactivity, underscoring the importance of considering APOE status when generating AD therapies. Polymorph-specific targeting of pathological tau species could provide a novel method of combating AD. HIGHLIGHTS: Conformational and bioactivity distinctions of tau oligomers have not yet been investigated across the APOE isoforms (ε2, ε3, ε4). Tau oligomers differ in conformational properties across the APOE isoforms. APOE ε4-relevant tau oligomers strongly impair synaptic plasticity and demonstrate high tau seeding activity. APOE ε4-relevant tau oligomers exist as a particularly toxic species, making them an ideal target for tau-based AD therapies.

Indexed as

Alzheimer DiseaseApolipoproteins ESynapsestau ProteinsAgedAnimalsFemaleHumansMaleProtein IsoformsApolipoproteins EProtein Isoformstau Proteinsaggregationoligomerspolymorphssynaptic functioningsynaptotoxicitytau

Identifiers

PMID41388809
PMCPMC12701364

What Socratic holds

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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 Socratic graph.