ReviewFrontiers in cellular neuroscience2015
Neuroinflammation in Multiple System Atrophy: Response to and Cause of α-Synuclein Aggregation.
Review in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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Who cites it
63 citing papers in PubMed, 90 citations in OpenAlex.
- Drug repurposing for disease-modifying effects in multiple system atrophy.Translational neurodegeneration · 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
- Multiple system atrophy: integrating clinical phenotypes and multimodal biomarkers for early diagnosis.Frontiers in aging neuroscience · 2026Review
- Development of convolutional neural networks for automated brain-wide histopathological analysis in mouse models of synucleinopathies.NPJ Parkinson's disease · 2025Article
- Optical coherence tomography reveals retinal structural abnormalities in α-synucleinopathies: insights from the Padua-CESNE cohort.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- The Inflammatory Mechanism of Parkinson's Disease: Gut Microbiota Metabolites Affect the Development of the Disease Through the Gut-Brain Axis.Brain sciences · 2025Review
- GFAP and NfL as fluid biomarkers for clinical disease severity and disease progression in multiple system atrophy (MSA).Journal of neurology · 2024Article
- The 'α-synucleinopathy syndicate': multiple system atrophy and Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Multiple system atrophy: an update and emerging directions of biomarkers and clinical trials.Journal of neurology · 2024Review
- Diagnostic value and correlation analysis of serum cytokine levels in patients with multiple system atrophy.Frontiers in cellular neuroscience · 2024Article
- Mitigating neurodegenerative diseases: the protective influence of baicalin and baicalein through neuroinflammation regulation.Frontiers in pharmacology · 2024Review
- Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Is Hearing Loss a Risk Factor for Idiopathic Parkinson's Disease? An English Longitudinal Study of Ageing Analysis.Brain sciences · 2023Article
- Association of COVID-19 with Comorbidities: An Update.ACS pharmacology & translational science · 2023Review
- The link between neuroinflammation and the neurovascular unit in synucleinopathies.Science advances · 2023Review
- The genetic basis of multiple system atrophy.Journal of translational medicine · 2023Review
- The Peripheral Immune Traits Changed in Patients with Multiple System Atrophy.Brain sciences · 2023Article
- The Synucleins and the Astrocyte.Biology · 2023Review
- Inflammation in multiple system atrophy.Frontiers in immunology · 2023Review
- The potential convergence of NLRP3 inflammasome, potassium, and dopamine mechanisms in Parkinson's disease.NPJ Parkinson's disease · 2022Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple system atrophy (MSA) is a progressive neurodegenerative disease presenting with combinations of autonomic dysfunction, parkinsonism, cerebellar ataxia and/or pyramidal signs. Oligodendroglial cytoplasmic inclusions (GCIs) rich in α-synuclein (α-syn) constitute the disease hallmark, accompanied by neuronal loss and activation of glial cells which indicate neuroinflammation. Recent studies demonstrate that α-syn may be released from degenerating neurons to mediate formation of abnormal inclusion bodies and to induce neuroinflammation which, interestingly, might also favor the formation of intracellular α-syn aggregates as a consequence of cytokine release and the shift to a pro-inflammatory environment. Here, we critically review the relationships between α-syn and astrocytic and microglial activation in MSA to explore the potential of therapeutics which target neuroinflammation.
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Registered trials
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.