Evidence map›Paper›PMID 41168814›Full record

ArticleAlzheimer's research & therapy2025

Detecting limbic predominant neurodegenerative co-pathologies in vivo in Alzheimer's disease: magnetic resonance imaging markers, cognitive correlates, and prognosis.

Nils Richter, Oezguer A Onur, Gereon R Fink, Alzheimer’s Disease Neuroimaging Initiative*

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Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Nils RichterCognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Center Jülich, Jülich, Germany. n.richter@fz-juelich.de.
Oezguer A OnurCognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Center Jülich, Jülich, Germany.
Gereon R FinkCognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Center Jülich, Jülich, Germany.
Alzheimer’s Disease Neuroimaging Initiative*

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn Alzheimer's disease (AD), limbic non-AD co-pathologies are common and contribute to memory impairment and accelerated clinical progression. To date, in vivo biomarkers of these co-pathologies are lacking. Here, we examined whether specific regional gray matter (GM) atrophy patterns on magnetic resonance imaging (MRI) allow distinguishing between patients with 'pure' AD pathology and those with AD pathology and limbic non-AD co-pathologies (AD

methodsAtrophy patterns based on ante-mortem MRI scans of histopathologically confirmed 'pure' AD (n = 36) and AD

resultsHistopathologically confirmed AD

conclusionsThe data suggest that in MCI due to AD, additional non-AD limbic co-pathologies are associated with greater hippocampal but less cortical atrophy and more rapid clinical decline. In contrast, in mild dementia due to AD, hippocampal GM was not associated with prognosis. Instead, cortical degeneration appeared to drive clinical progression.

Indexed as

Alzheimer DiseaseCognitive DysfunctionLimbic SystemAgedAged, 80 and overAtrophyDisease ProgressionDNA-Binding ProteinsFemaleGray MatterHumansMagnetic Resonance ImagingMaleMiddle AgedNeuropsychological TestsPrognosisDNA-Binding ProteinsTARDBP protein, humantau ProteinsArgyrophilic grain diseaseBraak stagesDementiaLimbic predominant age-related TDP-43 encephalopathy (LATE)Mild cognitive impairmentTau-proteinVoxel-based morphometry

Identifiers

PMID41168814
PMCPMC12573837

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