Evidence map›Paper›PMID 41636369›Full record

ArticleJournal of Alzheimer's disease : JAD2026

Incidence of altered proteins in the aging brain: Implications for biological diagnostic markers.

Irina Alafuzoff, Sylwia Libard

Abstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2026. 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. 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

2 authors.

Irina AlafuzoffDepartment of Pathology, Uppsala University Hospital, Uppsala, Sweden.
Sylwia LibardDepartment of Pathology, Uppsala University Hospital, Uppsala, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BackgroundIn aging-related neurodegeneration, therapeutic interventions directed at defined protein targets have been launched. A key step has been developing diagnostic biological markers, followed by immunotherapy. These steps have been achieved for amyloid-β protein (Aβ).ObjectiveTo evaluate, based on brain pathology, how frequently Aβ would be detectable in blood or cerebrospinal fluid in older individuals.MethodsWe assessed brain tissue from 1825 deceased subjects, 20% of whom were demented. We examined the presence of Aβ, hyperphosphorylated τ (HPτ), Transactive DNA-binding protein 43 (TDP-43), and α-synuclein (αS) using immunohistochemistry. The extent of these alterations was assessed following current consensus criteria.ResultsThe combination of Aβ/HPτ, constituting Alzheimer's disease neuropathological change (ADNC), was detected in 64% of subjects, increasing significantly (Pearson's Chi-Square

Indexed as

Agingalpha-SynucleinAmyloid beta-PeptidesDNA-Binding ProteinsNeurodegenerative DiseasesAgedAged, 80 and overAlzheimer DiseaseAutopsyBiomarkersBrainDementiaFemaleHumansImmunohistochemistryIncidencealpha-SynucleinAmyloid beta-PeptidesBiomarkersDNA-Binding ProteinsSNCA protein, humanTARDBP protein, humantau Proteinsagingalzheimer's diseaseamyloid-β proteinbiomarker relevancecognitive declinehyperphosphorylated τmixed proteinopathiestransactive DNA-binding protein 43α-synuclein

Identifiers

PMID41636369
PMCPMC12960740

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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.