ArticleTranslational psychiatry2020
Neuroinflammation in dementia with Lewy bodies: a human post-mortem study.
Article in Translational psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 79 citations in OpenAlex.
- Association of Plasma Phosphorylated Tau With the Response to Neflamapimod Treatment in Patients With Dementia With Lewy Bodies.Neurology · 2023Trial
- Disease-specific tau polymorphs are associated with unique protein networks across proteinopathies.The EMBO journal · 2026Article
- Deletion or immunotherapeutic blockade of FcγRIIb (CD32b) impairs α-Syn propagation in vivo.Acta neuropathologica · 2026Article
- Assessing subcortical, brainstem and cerebellar metabolic patterns using [18F]FDG PET-CT imaging in dementia with Lewy bodies.European journal of nuclear medicine and molecular imaging · 2026Article
- Neuronal titration of Snca via enhancer disruption mitigates disease onset in a Parkinson's disease mouse model.Brain : a journal of neurology · 2026Article
- Neuropathological correlates of imaging in dementia with Lewy bodies.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Blood-based immunophenotyping of T cell profiles in patients with neurodegenerative disorders.Alzheimer's research & therapy · 2026Article
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Plasma proteomics reveals divergent sex-specific senescence and bone biology signatures across neurodegenerative diseases.bioRxiv : the preprint server for biology · 2026Article
- Association between Human Leukocyte Antigen Alleles and Neuropathological Outcomes in Lewy Body Disease.Annals of neurology · 2026Article
- Peripheral and central inflammation associated with progressive cognitive decline in dementia with Lewy bodies.Brain communications · 2026Article
- Early Amyloid Formation and Neuroinflammatory Response in a Bigenic Mouse Model Expressing Human α-Synuclein and Aβ.Parkinson's disease · 2026Article
- Shared Neuroinflammatory Mechanisms Across Dementia Types: An Integrative Review.International journal of molecular sciences · 2025Review
- Molecular Crossroads: Shared and Divergent Molecular Signatures in Alzheimer's Disease and Dementia with Lewy Bodies.International journal of molecular sciences · 2025Review
- Next-generation neurotherapeutics: nanotechnology, immunotherapy, and gene editing for neurodegenerative diseases.Neurodegenerative disease management · 2025Review
- Integrative Mendelian randomization for detecting exposure-by-group interactions using group-specific and combined summary statistics.PLoS genetics · 2025Article
- Single-nucleus transcriptomics reveals a distinct microglial state and increased MSR1-mediated phagocytosis as common features across dementia subtypes.Genome medicine · 2025Article
- Differential roles of human tau isoforms in the modulation of inflammation and development of neuropathology.Neurobiology of disease · 2025Article
- Current strategies in the management of dementia with lewy bodies and future directions based on disease pathophysiology.Molecular neurodegeneration · 2025Review
- Hypometabolic mismatch with atrophy and tau pathology in mixed Alzheimer's and Lewy body disease.Brain : a journal of neurology · 2025Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Dementia with Lewy bodies (DLB) is the second most common neurodegenerative cause of dementia, behind Alzheimer's disease (AD). It is now established that cerebral inflammation has a key role in the aetiology and progression of AD, but this has yet to be confirmed in DLB. We aimed to determine the neuroinflammatory profile in the cerebral cortex of a large cohort of DLB cases. Thirty post-mortem confirmed DLB cases and twenty-nine matched controls were immunolabelled (Brodmann area 21) and quantified for: neuropathology-αSYN, Aβ, P-tau; microglial phenotype-Iba1, HLA-DR, CD68, FcƴR (CD64, CD32a, CD32b, CD16); presence of T lymphocytes-CD3; and anti-inflammatory markers-IL4R, CHI3L1. Status spongiosis, as a marker of neuropil degeneration, was quantified using Haematoxylin and Eosin staining. We found no significant difference between groups in protein load for Iba1, HLA-DR, CD68, CD64, CD32b, IL4R, or CHI3L1, despite increased neuropathology in DLB. CD32a load was significantly lower, and CD16 load higher, in DLB compared with controls. There was no difference in status spongiosis between groups. Significantly more DLB cases than controls showed T-lymphocyte recruitment. Overall, we conclude that microglial activation is not a prominent feature of DLB, and that this may be associated with the relatively modest neuropil degeneration observed in DLB. Our findings, based on the largest post-mortem cohort to date exploring neuroinflammation in DLB, demonstrate a dissociation between protein deposition, neurodegeneration and microglial activation. The relative preservation of cortical structures in DLB suggests the dementia could be more amenable to potential therapies.
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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.