Evidence map›Paper›PMID 42529064›Full record

ArticleBrain communications2026

Peripheral and central inflammation associated with progressive cognitive decline in dementia with Lewy bodies.

Peter Swann, Maura Malpetti, Leonidas Chouliaras, Simon R White, Elijah Mak, Ajenthan Surendranathan, P Simon Jones, Li Su, George Savulich, Stacey Kigar and 6 more

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Article in Brain communications, 2026. 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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2 · The registry

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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

16 authors.

Peter SwannDepartment of Psychiatry, University of Cambridge, Cambridge CB2 0QQ, UK.
Maura MalpettiDepartment of Clinical Neurosciences and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge CB2 0SZ, UK.ORCID https://orcid.org/0000-0001-8923-9656
Leonidas ChouliarasDepartment of Psychiatry, University of Cambridge, Cambridge CB2 0QQ, UK.ORCID https://orcid.org/0000-0002-3052-3879
Simon R WhiteDepartment of Psychiatry, University of Cambridge, Cambridge CB2 0QQ, UK.
Elijah MakDepartment of Psychiatry, University of Cambridge, Cambridge CB2 0QQ, UK.ORCID https://orcid.org/0000-0002-6437-8024
Ajenthan SurendranathanNational Hospital for Neurology and Neurosurgery, University College Hospitals London, London WC1N 3BG, UK.
P Simon JonesDepartment of Clinical Neurosciences and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge CB2 0SZ, UK.
Li SuDepartment of Psychiatry, University of Cambridge, Cambridge CB2 0QQ, UK.
George SavulichDepartment of Psychiatry, University of Cambridge, Cambridge CB2 0QQ, UK.ORCID https://orcid.org/0000-0002-6513-5454
Stacey KigarDepartment of Psychiatry, University of Cambridge, Cambridge CB2 0QQ, UK.
Anna McKeeverDepartment of Psychiatry, University of Cambridge, Cambridge CB2 0QQ, UK.
Tim FryerDepartment of Clinical Neurosciences and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge CB2 0SZ, UK.
Young T HongDepartment of Clinical Neurosciences and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge CB2 0SZ, UK.
Franklin I AigbirhioDepartment of Clinical Neurosciences and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge CB2 0SZ, UK.
James B RoweDepartment of Clinical Neurosciences and Cambridge University Hospitals NHS Trust, University of Cambridge, Cambridge CB2 0SZ, UK.
John T O'BrienDepartment of Psychiatry, University of Cambridge, Cambridge CB2 0QQ, UK.ORCID https://orcid.org/0000-0002-0837-5080

Funding

Wellcome Trust
6 · The paper itself

Abstract

Dementia with Lewy bodies (DLB) is the second most common cause of neurodegenerative dementia, pathologically defined by the presence of Lewy bodies. Peripheral and central inflammation are increasingly recognized in DLB in clinical, post-mortem and animal studies. Finding clinically relevant biomarkers of inflammation in DLB will support the identification of novel pathways for disease-modifying therapies or use in clinical trials of immunomodulatory agents. Whilst there are cross-sectional studies of inflammation markers in DLB, there is limited evidence on the association between these markers and cognitive decline over time. Twenty participants with DLB underwent blood sampling for serum inflammatory markers, paired with PET imaging of the translocator protein (TSPO) and up to 4 years of longitudinal cognitive testing. Thirty participants with Alzheimer's disease-comprising both Alzheimer's dementia and/or mild cognitive impairment with biomarker evidence of amyloid pathology (AD/MCI+)-and 28 controls were also recruited for group comparisons. Data from 42 baseline cytokine immunoassays and TSPO PET were used as predictors of longitudinal cognitive scores in linear mixed-effects models. Partial least squares regression was used to test the association between peripheral and central inflammation. Using peripheral inflammatory markers as single predictors, we identified 14 associated with either a slower or faster rate of cognitive decline in DLB, whilst no single marker was predictive of decline in AD/MCI+. As many inflammatory markers were highly correlated, we used principal component analysis to identify a cytokine component associated with reduced cognitive decline in both DLB and AD/MCI+, that overlapped with the single markers identified in the previous analysis. A separate component was associated with cognitive decline in AD/MCI+ or DLB with Alzheimer's dementia co-pathology (ascertained by amyloid PET). Widespread TSPO binding was associated with reduced cognitive decline in DLB, whilst a fronto-temporal pattern was associated with more rapid cognitive decline in both DLB and AD/MCI+. There were associations between peripheral cytokines and TSPO PET in AD/MCI+, but these were not significant in DLB. Overall, peripheral and central inflammation predicted cognitive decline in DLB. Specific patterns associated with both faster and slower rates of decline were identified. These profiles had both overlapping and contrasting associations when compared to AD/MCI+. Collectively, these data add to a body of evidence suggesting clinically relevant levels of inflammation in DLB. Future studies in larger, multi-site cohorts with multiple biomarker sampling points are required to understand the impact and dynamics of inflammation across all stages of the disease.

Indexed as

cognitiondementiainflammationLewylongitudinal

Identifiers

PMID42529064
PMCPMC13416190

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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.