ReviewFrontiers in immunology2024
Inflammation and heterogeneity in synucleinopathies.
Review in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- When Pathologies Collide: The Intersection of Tau and Alpha-Synuclein in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Lysophospholipids in Synucleinopathies: A Conceptual Framework Linking Proteostasis and Neuroinflammatory Signaling.Brain sciences · 2026Review
- Cytotoxic T cell recognition of α-synuclein drives pathogenic immune responses in multiple system atrophy.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Propagation of α-synuclein pathology: models, mechanisms and future goals.Molecular neurodegeneration advances · 2026Review
- Gut-brain immune dysregulation in Parkinson's disease: a hypothesis-forming narrative review of trained immunity.Frontiers in aging neuroscience · 2026Review
- Sex-dependent immune activation shapes disease progression in a model of Parkinson's disease.Biology of sex differences · 2025Article
- "Recommendations for clinical study protocols for immune and inflammatory profiling in Parkinson's disease".NPJ Parkinson's disease · 2025Review
- Article
- T cell responses towards PINK1 and α-synuclein are elevated in prodromal Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Differential memory enrichment of cytotoxic CD4 T cells in Parkinson's disease patients reactive to α-synuclein.NPJ Parkinson's disease · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegenerative diseases represent a huge healthcare challenge which is predicted to increase with an aging population. Synucleinopathies, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), present complex challenges in understanding their onset and progression. They are characterized by the abnormal aggregation of α-synuclein in the brain leading to neurodegeneration. Accumulating evidence supports the existence of distinct subtypes based on the site of α-synuclein aggregation initiation, genetics, and, more recently, neuroinflammation. Mediated by both central nervous system-resident cells, peripheral immune cells, and gut dysbiosis, neuroinflammation appears as a key process in the onset and progression of neuronal loss. Sex-based differences add another layer of complexity to synucleinopathies, influencing disease prevalence - with a known higher incidence of PD in males compared to females - as well as phenotype and immune responses. Biological sex affects neuroinflammatory pathways and the immune response, suggesting the need for sex-specific therapeutic strategies and biomarker identification. Here, we review the heterogeneity of synucleinopathies, describing the etiology, the mechanisms by which the inflammatory processes contribute to the pathology, and the consideration of sex-based differences to highlight the need for personalized therapeutics.
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