ReviewNeuroscience bulletin2023
Association of Glial Activation and α-Synuclein Pathology in Parkinson's Disease.
Review in Neuroscience bulletin, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Association of chronic pain and analgesic use with the risks of Parkinson's and Alzheimer's disease.GeroScience · 2026Article
- Review
- Potential Transmission of Alpha-Synuclein from the Gastrointestinal Tract to the Substantia Nigra along the Vagal Afferent Pathway.Neuroscience bulletin · 2026Article
- Role of Microglial Dysfunction in Parkinson's Disease: From Multifactorial Causes to Neurodegeneration.Neuroscience bulletin · 2026Review
- Targeting the cardio-neuro axis through nutrition: inflammatory mechanisms linking cardiovascular and neurodegenerative diseases.Frontiers in nutrition · 2026Article
- From retina to brain: retinal dysfunction and dopaminergic neurodegeneration inFrontiers in cell and developmental biology · 2026Article
- Cellular Communication Networks Mediated by Microglia in Ischemic Stroke.CNS neuroscience & therapeutics · 2025Review
- Bridging the Gap: The Neuro-immune Axis as a Key Player in Neurodegenerative Disorders.Neuroscience bulletin · 2025Review
- The IL-12 family cytokines in neurodegenerative diseases: dual roles in neurotoxicity and neuroprotection.Inflammopharmacology · 2025Review
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Gut Microbiota-Based Interventions for Parkinson's Disease: Neuroprotective Mechanisms and Current Perspective.Probiotics and antimicrobial proteins · 2025Review
- Relationships between neuropsychiatric symptoms, subtypes of astrocyte activities, and brain pathologies in Alzheimer's disease and Parkinson's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Chronic Vanadium Exposure Promotes Aggregation of Alpha-Synuclein, Tau and Amyloid Beta in Mouse Brain.Journal of neurochemistry · 2025Article
- Loss of NgBR causes neuronal damage through decreasing KAT7-mediated RFX1 acetylation and FGF1 expression.Cellular and molecular life sciences : CMLS · 2025Article
- The Role and Mechanisms of Ubiquitin-Proteasome System-Mediated Ferroptosis in Neurological Disorders.Neuroscience bulletin · 2025Review
- Type 2 Diabetes Mellitus Exacerbates Pathological Processes of Parkinson's Disease: Insights from Signaling Pathways Mediated by Insulin Receptors.Neuroscience bulletin · 2025Review
- Article
- Chronic DSS-Induced Colitis Exacerbates Parkinson's Disease Phenotype and Its Pathological Features Following Intragastric Rotenone Exposure.ACS pharmacology & translational science · 2025Article
- Novel Glitazones Protect Rotenone-induced Parkinsonism in Mouse Models by Targeting PGC1α.Current drug targets · 2025Article
- Accumulation of Alpha-Synuclein and Increase in the Inflammatory Response in theInternational journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The accumulation of pathological α-synuclein (α-syn) in the central nervous system and the progressive loss of dopaminergic neurons in the substantia nigra pars compacta are the neuropathological features of Parkinson's disease (PD). Recently, the findings of prion-like transmission of α-syn pathology have expanded our understanding of the region-specific distribution of α-syn in PD patients. Accumulating evidence suggests that α-syn aggregates are released from neurons and endocytosed by glial cells, which contributes to the clearance of α-syn. However, the activation of glial cells by α-syn species produces pro-inflammatory factors that decrease the uptake of α-syn aggregates by glial cells and promote the transmission of α-syn between neurons, which promotes the spread of α-syn pathology. In this article, we provide an overview of current knowledge on the role of glia and α-syn pathology in PD pathogenesis, highlighting the relationships between glial responses and the spread of α-syn pathology.
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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.