Evidence map›Paper›PMID 42839194›Full record

ArticleJournal of neurology2026

Cortical thickness signature of early-onset Alzheimer's disease across clinical stages and A/T1 biomarker profiles.

Alessandro Zilioli, Rosaleena Mohanty, Anna Rosenberg, Anna Matton, Tobias Granberg, Göran Hagman, Marco Spallazzi, Miia Kivipelto, Eric Westman

Abstract read
In one paragraph

Article in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Alessandro ZilioliDepartment of Neurology, University-Hospital of Parma, Parma, Italy. Alessandro.zilioli@ki.se.
Rosaleena MohantyDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Stockholm, Sweden.
Anna RosenbergDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Stockholm, Sweden.
Anna MattonDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Stockholm, Sweden.
Tobias GranbergDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Göran HagmanDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Stockholm, Sweden.
Marco SpallazziDepartment of Neurology, University-Hospital of Parma, Parma, Italy.
Miia Kivipelto *Division of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Stockholm, Sweden.
Eric Westman *Division of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Stockholm, Sweden. eric.westman@ki.se.ORCID http://orcid.org/0000-0002-3115-2977

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe cortical thinning signature of early-onset Alzheimer's disease (EOAD) is well established in dementia, but its emergence during earlier disease stages remains unclear. We investigated when it becomes detectable and whether it differs according to fluid amyloid and phosphorylated-tau (A/T1) biomarker profiles.

methodsWe studied 292 individuals <65 years who underwent 3T structural MRI and cerebrospinal fluid assessment of Aβ42/40 and p-tau181. Participants were classified as A-T1- subjective cognitive decline (SCD; reference group), A+T1-, or A+T1+. Cortical thickness and hippocampal volume were measured using FreeSurfer. EOAD signature regions were defined by comparing biomarker-confirmed AD dementia with the reference group and subsequently examined across A/T1 profiles in SCD and mild cognitive impairment (MCI). Brain-cognition associations were assessed.

resultsThe cohort comprised 107 reference and 185 amyloid-positive participants (76 A+T1- and 109 A+T1+). EOAD dementia was characterized by marked cortical thinning in posterior parietal and lateral temporal regions. In MCI, cortical thinning was focal in A+T1-, but more extensive in A+T1+ who also showed hippocampal atrophy. At the SCD stage, focal thinning of the EOAD signature, precuneus, and banks of the superior temporal sulcus was observed in A+T1+, whereas no structural alterations were detected in A+T1-. Cortical thinning was associated with episodic and visuospatial memory performance in MCI, while no brain-cognition associations were observed in SCD.

conclusionEOAD-related cortical thinning is detectable before dementia and varies across A/T1 profiles, with combined amyloid and p-tau181 positivity associated with earlier and more extensive structural involvement.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCerebral CortexCerebral Cortical ThinningCognitive DysfunctionPeptide Fragmentstau ProteinsBiomarkersDisease ProgressionFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)BiomarkersMAPT protein, humanPeptide Fragmentstau ProteinsA/T1 biomarker profilesCortical thicknessEarly-onset Alzheimer’s diseaseMild cognitive impairmentSubjective cognitive decline

Identifiers

PMID42839194
PMCPMC13642493

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.