Evidence map›Paper›PMID 42363728›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

Inflammation profiles in Alzheimer's disease relate to cognition and neurodegeneration.

Katherine R Birditt, Kalliopi Mavromati, Peter Swann, Terence Quinn, Atticus H Hainsworth, Lynne Hughes, John T O'Brien, William McEwan, Maura Malpetti

Abstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 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.

Katherine R BirdittDepartment of Clinical Neurosciences, University of Cambridge and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge, UK.ORCID https://orcid.org/0009-0002-9783-8012
Kalliopi MavromatiSchool of Cardiovascular and Metabolic Health, University of Glasgow, Glasgow, UK.
Peter SwannDepartment of Psychiatry, School of Clinical Medicine, University of Cambridge, Cambridge, UK.
Terence QuinnSchool of Cardiovascular and Metabolic Health, University of Glasgow, Glasgow, UK.
Atticus H HainsworthMolecular and Clinical Sciences Research Institute, St George's University of London, London, UK.
Lynne HughesGlobal Alzheimer's Platform Foundation, Washington, Washington DC, USA.
John T O'BrienDepartment of Psychiatry, School of Clinical Medicine, University of Cambridge, Cambridge, UK.
William McEwanDepartment of Clinical Neurosciences, University of Cambridge and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge, UK.
Maura MalpettiDepartment of Clinical Neurosciences, University of Cambridge and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge, UK.

Funding

Medical Research CouncilNational Institute for Health Research (NIHR) Cambridge Biomedical Research Centre NIHR203312Race Against Dementia Alzheimer's Research UK ARUK-RADF2021A-010
6 · The paper itself

Abstract

introductionImmune signaling alterations have been implicated in Alzheimer's disease (AD) pathophysiology, but their heterogeneity across the disease continuum in real-world cohorts is poorly characterized, limiting the development of stratified immunomodulatory approaches.

methodsIn a diverse multicenter cohort (BioHermes) of 176 amyloid-positive individuals with AD/mild cognitive impairment (MCI) and 173 age and sex-matched controls, principal component analysis was performed on Luminex-measured plasma cytokines to derive inflammatory signatures, and their direct/indirect associations with cognition and neurodegeneration.

resultsTwo components were identified. Proinflammatory Component 2 was elevated in AD/MCI and in Black/African American participants, and strongly associated with poorer cognition (independently of neurofilament light [NfL], phosphorylated tau 217 [p-tau217], and glial fibrillary acidic protein [GFAP]). Inflammatory Component 1 showed an indirect association with cognition, mediated by neurodegeneration (plasma NfL). DISCUSSION: Plasma inflammation profiles were associated with poorer cognition via direct and neurodegeneration-mediated pathways, supporting their potential use as stratification markers in AD therapeutics.

Indexed as

Alzheimer DiseaseCognitionCognitive DysfunctionCytokinesInflammationAgedAged, 80 and overBiomarkersCohort StudiesFemaleHumansMaleNeurofilament Proteinstau ProteinsBiomarkersCytokinesneurofilament protein LNeurofilament Proteinstau ProteinsAlzheimer's diseaseblood‐based biomarkerscytokinesmultiplex assaysneurodegenerative diseasesneuroinflammation

Identifiers

PMID42363728
PMCPMC13309851

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.