Evidence map›Paper›PMID 39711489›Full record

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

Co-pathologies modify hippocampal protein accumulation patterns in neurodegenerative diseases.

Koji Yoshida, Shelley L Forrest, Shojiro Ichimata, Hidetomo Tanaka, Tomoya Kon, Gabor G Kovacs

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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
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  7. Co-pathologies modify hippocampal protein accumulation patterns in neurodegenerative diseases.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

6 authors.

Koji YoshidaDepartment of Laboratory Medicine and Pathobiology and Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
Shelley L ForrestDepartment of Laboratory Medicine and Pathobiology and Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
Shojiro IchimataDepartment of Laboratory Medicine and Pathobiology and Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
Hidetomo TanakaDepartment of Laboratory Medicine and Pathobiology and Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
Tomoya KonDepartment of Laboratory Medicine and Pathobiology and Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
Gabor G KovacsDepartment of Laboratory Medicine and Pathobiology and Department of Medicine, University of Toronto, Toronto, Ontario, Canada.ORCID 0000-0003-3841-5511

Funding

Canadian Foundation for Innovation 40480Edmond J. Safra Philanthropic FoundationOntario Research FundRossy Family Foundation
6 · The paper itself

Abstract

introductionLimited research has extensively analyzed neurodegenerative disease-related protein deposition patterns in the hippocampus.

methodsThis study examined the distribution of proteins in hippocampal subregions across major neurodegenerative diseases and explored their relation to each other. The area density of phosphorylated tau (p-tau), amyloid beta (Aβ), α-synuclein, and phosphorylated TDP-43 protein deposits together with pyramidal cell density in each hippocampal subregion, including CA1-4, prosubiculum (ProS), and subiculum was assessed in 166 cases encompassing various neurodegenerative diseases.

resultsAlzheimer's disease-associated p-tau predominated in ProS, Aβ in the CA1, and Lewy body-related α-synuclein in the CA2. The area density of protein deposits increased with the pathological stage until a peak, then decreased in cases with high pathology stages along with pyramidal cell density. Comorbid protein pathology influenced protein deposition patterns. DISCUSSION: This comprehensive evaluation reveals characteristic neurodegenerative disease-related protein accumulation patterns in hippocampal subregions modified by co-pathologies. HIGHLIGHTS: Alzheimer's disease-related phosphorylated tau predominates in the prosubiculum. Amyloid beta predominates in the CA1 and Lewy body-related α-synuclein in the CA2. The area density of protein deposition increases with the disease stage up to a peak. In the high pathology stage, protein deposition and pyramidal cell density decreases. Comorbid protein pathology affects the pattern of protein accumulation.

Indexed as

HippocampusNeurodegenerative DiseasesAgedAged, 80 and overalpha-SynucleinAlzheimer DiseaseAmyloid beta-PeptidesDNA-Binding ProteinsFemaleHumansMaleMiddle AgedPhosphorylationPyramidal Cellstau Proteinsalpha-SynucleinAmyloid beta-PeptidesDNA-Binding ProteinsTARDBP protein, humantau Proteinsalpha‐synucleinAlzheimer's diseaseamyloid betacorticobasal degenerationhippocampusLewy body diseaselimbic predominant age‐related TDP‐43 encephalopathy neuropathological changephosphorylated tauprogressive supranuclear palsyTDP‐43

Identifiers

PMID39711489
PMCPMC11782183

What Socratic holds

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LicenceCC BY
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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 Socratic graph.