ReviewJournal of neurochemistry2025
Clearance Pathways for α-Synuclein in Parkinson's Disease.
Review in Journal of neurochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- Symptomatic Rescue or Disease Modification? A Critical Review of Levodopa and Phytochemical Interventions in Caenorhabditis elegans Models of Parkinson's Disease.Molecular neurobiology · 2026Review
- Convergent Astrocytic Failure in Parkinson's Disease: A System-Level Model of Pathogenesis and Treatment.Molecular neurobiology · 2026Review
- A new paradigm in Parkinson's disease: kidney-origin α-synuclein pathology driven by PKC signaling and aurothioglucose.Inflammopharmacology · 2026Review
- Lysosomal homeostasis at the crossroads of neurodegeneration.The Journal of clinical investigation · 2026Review
- Copper Dyshomeostasis Affects α-Synuclein Clearance Mechanisms in Parkinson's Disease: Insights from In Vitro Models and Translational Evidence.International journal of molecular sciences · 2026Review
- Beyond Pathology: α-Synuclein Homeostasis and Three Principles to Guide Research.Movement disorders clinical practice · 2026Article
- Glial-Dopamine crosstalk: Astrocytic and microglial gatekeepers of neuroinflammation, plasticity, and motivation.AIMS neuroscience · 2026Review
- GLP-1 Receptor Agonists in Neurological Disorders: From Mechanisms to Clinical Translation.Drug design, development and therapy · 2026Review
- Propagation of α-synuclein pathology: models, mechanisms and future goals.Molecular neurodegeneration advances · 2026Review
- "Rewiring brain immunity: targeting microglial metabolism for neuroprotection in neurodegenerative disorders".Metabolic brain disease · 2025Review
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Protein aggregation and accumulation are hallmark features of neurodegenerative diseases. In Parkinson's disease, the progressive formation and propagation of α-synuclein aggregates-found in Lewy bodies and Lewy neurites-are closely linked to widespread neuronal dysfunction, dopaminergic neuron loss, and the emergence of both motor and nonmotor symptoms, including anosmia, cognitive decline, and depression. Despite their pathological significance, the mechanisms underlying the formation, spread, and clearance of these aggregates remain incompletely understood. In this review, we examine the cellular and molecular pathways responsible for the elimination of protein aggregates in the diseased brain. We first summarize various experimental models of α-synuclein pathology, followed by a discussion of the degradation mechanisms in neurons and glial cells under pathological conditions. These findings offer new insights into cell type-specific clearance pathways and highlight potential therapeutic targets for mitigating α-synuclein-associated toxicity in Parkinson's disease.
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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.