ArticleScientific reports2023
Elevated GRO-α and IL-18 in serum and brain implicate the NLRP3 inflammasome in frontotemporal dementia.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Pooled it
- Loss of Progranulin Expression Decreases NLRP3 Inflammasome-Mediated Inflammation and Enhances Bone Anabolism.Research square · 2026Article
- Peripheral immune profiling in frontotemporal dementia.Brain communications · 2026Article
- Glial activation and increase in cerebral pro-inflammatory cytokine expression in a female animal post-COVID model.Brain, behavior, & immunity - health · 2025Article
- The NLRP3 inflammasome: a pivotal orchestrator of multisystem diseases-from molecular mechanisms to therapeutic innovation.Molecular biology reports · 2025Review
- Eosinophil recruitment and activation in the central nervous system of patients with subarachnoid neurocysticercosis.Journal of neuroinflammation · 2025Article
- The IL-12 family cytokines in neurodegenerative diseases: dual roles in neurotoxicity and neuroprotection.Inflammopharmacology · 2025Review
- Alzheimer's disease neuropathology and its estimation with fluid and imaging biomarkers.Molecular neurodegeneration · 2025Review
- Immunological aspects of central neurodegeneration.Cell discovery · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation is a hallmark of frontotemporal dementia (FTD), a heterogeneous group of proteinopathies characterized by the progressive degeneration of the frontal and temporal lobes. It is marked by microglial activation and subsequent cytokine release. Although cytokine levels in FTD brain and CSF have been examined, the number of cytokines measured in each study is limited and knowledge on cytokine concentrations in FTD serum is scarce. Here, we assessed 48 cytokines in FTD serum and brain. The aim was to determine common cytokine dysregulation pathways in serum and brain in FTD. Blood samples and brain tissue samples from the superior frontal cortex (SFC) were collected from individuals diagnosed with behavioral variant FTD (bvFTD) and healthy controls, and 48 cytokines were measured using a multiplex immunological assay. The data were evaluated by principal component factor analysis to determine the contribution from different components of the variance in the cohort. Levels of a number of cytokines were altered in serum and SFC in bvFTD compared to controls, with increases in GRO-α and IL-18 in both serum and SFC. These changes could be associated with NLRP3 inflammasome activation or the NFκB pathway, which activates NLRP3. The results suggest the possible importance of the NLRP3 inflammasome in FTD. An improved understanding of the role of inflammasomes in FTD could provide valuable insights into the pathogenesis, diagnosis and treatment of FTD.
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