Evidence map›Paper›PMID 41298940›Full record

ArticleActa neuropathologica2025

Neuropathologic correlates of cognitive impairment in Alzheimer's disease with discordant CSF biomarker profiles: co-pathologies in focus.

Konstantinos Ioannou, Richard J Perrin, Khadidzha Abdullaieva, Marina Bluma, Antoine Leuzy, Konstantinos Poulakis, Dorota Religa, Elena Rodriguez-Vieitez, Konstantinos Chiotis, Alzheimer’s Disease Neuroimaging Initiative

Abstract read
In one paragraph

Article in Acta neuropathologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Multimodal axes reveal individualized amyloid-medRxiv : the preprint server for health sciences · 2026
    Article
  4. 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

10 authors.

Konstantinos IoannouDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Neo 7Th Floor 141 52, Huddinge, Stockholm, Sweden.
Richard J PerrinKnight Alzheimer Disease Research Center, Washington University School of Medicine, Saint Louis, USA.
Khadidzha AbdullaievaDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Neo 7Th Floor 141 52, Huddinge, Stockholm, Sweden.
Marina BlumaDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Neo 7Th Floor 141 52, Huddinge, Stockholm, Sweden.
Antoine LeuzyCenter for Age-Related Diseases, Stavanger University Hospital, Stavanger, Norway.
Konstantinos PoulakisDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Neo 7Th Floor 141 52, Huddinge, Stockholm, Sweden.
Dorota ReligaDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Neo 7Th Floor 141 52, Huddinge, Stockholm, Sweden.
Elena Rodriguez-VieitezDivision of Neurogeriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Konstantinos ChiotisDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Neo 7Th Floor 141 52, Huddinge, Stockholm, Sweden. konstantinos.chiotis@ki.se.
Alzheimer’s Disease Neuroimaging Initiative

Funding

Project 1U19AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI MONICA G. RIVERA-MINDT · 2016 to 2026
$226.7M
NIA NIH HHS U19 AG024904
6 · The paper itself

Abstract

CSF Aβ reflects Alzheimer's disease neuropathologic change (ADNC), while CSF p-tau offers an indirect indication of tangle pathology. However, interpretation can be challenging when cognitive impairment is present alongside Aβ positivity (Α +) but p-tau negativity (T -). We examined neuropathologic differences between CSF A + T - and A + T + profiles, defined by CSF Aβ42 and p-tau181 levels, hypothesizing that cognitively impaired older adults with a CSF A + T - profile would exhibit a greater co-pathology burden, suggesting alternative contributing disease processes. We identified 77 ADNI participants with available CSF biomarkers and neuropathologic assessments (median age = 79.8 years; IQR = 74.7-84.5). Depending on the presence-alone or in combination-of ADNC intermediate/high and non-ADNC pathologies (e.g., Lewy bodies (LB), argyrophilic grain disease (AGD), limbic-predominant age-related TDP-43 encephalopathy-neuropathologic change (LATE-NC)), individuals were classified as ADNC dominant, mixed ADNC, or non-ADNC dominant. The two CSF A + profiles were similar in demographics, frequency of cognitive impairment, longitudinal cognitive performance, clinical comorbidities, CSF Aβ42 levels, CSF α-synuclein positivity rates, and Aβ PET burden. ADNC intermediate/high was significantly more frequent in the CSF A + T + profile than in the CSF A + T - profile (100% vs. 78%, p value = 0.008). The most common co-pathologies contributing to cognitive impairment in the CSF A + T - profile were LATE-NC (stages 2-3) (47%), LB limbic/neocortical (44%), and AGD (stages II-III) (33%), while in the CSF A + T + profile, LB limbic/neocortical (28%) and LATE-NC (stages 2-3) (22%) predominated. The CSF A + T - profile showed 17% ADNC dominant, 61% mixed ADNC, and 22% non-ADNC dominant pathology, whereas the CSF A + T + profile showed 51% ADNC dominant and 49% mixed ADNC pathology (p = 0.001). Within the mixed ADNC subgroup, individuals with a CSF A + T - profile more often exhibited two or more non-ADNC co-pathologies compared to those with a CSF A + T + profile (73% vs. 21%, p = 0.009). Despite clinical similarities among cognitively impaired individuals with CSF A + T - and A + T + profiles, the CSF A + T - profile may reflect a greater burden of non-ADNC pathology. Extending biomarker profiling beyond Aβ and tau may facilitate more personalized care.

Indexed as

Alzheimer DiseaseBrainCognitive DysfunctionAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersFemaleHumansMalePeptide Fragmentstau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersPeptide Fragmentstau ProteinsADNCAlzheimerAT biomarker systemCo-pathologiesCSFp-tauβ-amyloid

Identifiers

PMID41298940
PMCPMC12657578

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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.