Evidence map›Paper›PMID 40400344›Full record

ArticleJournal of Alzheimer's disease : JAD2025

Neural mechanisms of disease pathology and cognition in young-onset Alzheimer's disease variants.

Seda Sacu, Catherine F Slattery, Karl J Friston, Ross W Paterson, Alexander Jm Foulkes, Keir Yong, Sebastian Crutch, Jonathan M Schott, Adeel Razi

Abstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2025. 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. 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

9 authors.

Seda SacuCentral Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.ORCID 0000-0003-4734-9835
Catherine F SlatteryDepartment of Neurodegenerative Disease, Institute of Neurology, University College London, London, UK.
Karl J FristonWellcome Centre for Human Neuroimaging, Institute of Neurology, University College London, London, UK.
Ross W PatersonDepartment of Neurodegenerative Disease, Institute of Neurology, University College London, London, UK.
Alexander Jm FoulkesDepartment of Neurodegenerative Disease, Institute of Neurology, University College London, London, UK.
Keir YongDepartment of Neurodegenerative Disease, Institute of Neurology, University College London, London, UK.
Sebastian CrutchDepartment of Neurodegenerative Disease, Institute of Neurology, University College London, London, UK.
Jonathan M SchottDepartment of Neurodegenerative Disease, Institute of Neurology, University College London, London, UK.
Adeel RaziWellcome Centre for Human Neuroimaging, Institute of Neurology, University College London, London, UK.

Funding

Wellcome Trust
6 · The paper itself

Abstract

BackgroundLate-onset Alzheimer's disease is consistently associated with alterations in the default-mode network (DMN)-a large-scale brain network associated with self-related processing and memory. However, the functional organization of DMN is far less clear in young-onset Alzheimer's disease (YOAD).ObjectiveThe current study aimed to identify effective connectivity changes in the core DMN nodes between YOAD variants and healthy controls.MethodsWe assessed resting-state DMN effective connectivity in two common YOAD variants (i.e., amnestic variant (n = 26) and posterior cortical atrophy (n = 13) and healthy participants (n = 24) to identify disease- and variant-specific connectivity differences using spectral dynamic causal modelling.ResultsPatients with the amnestic variant showed increased connectivity from prefrontal cortex to posterior DMN nodes relative to healthy controls, whereas patients with posterior cortical atrophy exhibited decreased posterior DMN connectivity. Right hippocampus connectivity differentiated the two patient groups. Furthermore, disease-related connectivity alterations were also predictive of group membership and cognitive performance.ConclusionsThese findings suggest that resting-state DMN effective connectivity provides a new understanding of neural mechanisms underlying the disease pathology and cognition in YOAD.

Indexed as

Alzheimer DiseaseBrainCognitionAge of OnsetAtrophyFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedNeuropsychological TestsAlzheimer's diseasedynamic causal modellingearly-onset Alzheimer's diseaseeffective connectivityposterior cortical atrophyresting-state fMRIyoung-onset Alzheimer's disease

Identifiers

PMID40400344
PMCPMC12227830

What Socratic holds

Textmetadata
LicenceCC BY-NC
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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 Socratic graph.