ReviewFrontiers in cellular neuroscience2022
The role of the endolysosomal pathway in α-synuclein pathogenesis in Parkinson's disease.
Review in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Reducing PI4KIIIα Levels or Activity Limits Tau Seed Internalization and Assembly in Human Cortical Neurons.Cells · 2026Article
- Targeting protein aggregate co-pathologies in neurodegeneration: a viable therapeutic strategy?Molecular neurodegeneration advances · 2026Review
- Underlying Mechanisms of GBA1 in Parkinson's Disease and Dementia with Lewy Bodies: Narrative Review.Genes · 2025Review
- LRRK2 kinase-mediated accumulation of lysosome-associated phospho-Rabs in tauopathies and synucleinopathies.Acta neuropathologica · 2025Article
- The Comorbidity of AD and PD: Exploring Clinical, Pathological, and Biomarker Interactions.Aging and disease · 2025Review
- Plasma Metabolites as Mediators Between Gut Microbiota and Parkinson's Disease: Insights from Mendelian Randomization.Molecular neurobiology · 2025Article
- Endocytic Pathways Unveil the Role of Syndecans in the Seeding and Spreading of Pathological Protein Aggregates: Insights into Neurodegenerative Disorders.International journal of molecular sciences · 2025Review
- Emerging targets of α-synuclein spreading in α-synucleinopathies: a review of mechanistic pathways and interventions.Molecular neurodegeneration · 2025Review
- Dysregulation of protein degradation and alteration of secretome in α-synuclein-exposed astrocytes: implications for dopaminergic neuronal dysfunction.Cell communication and signaling : CCS · 2024Article
- In situ stoichiometry amounts of p62 and poly-ubiquitin exceed the increase of alpha-synuclein during degeneration of catecholamine cells induced by autophagy inhibition in vitro.Journal of neural transmission (Vienna, Austria : 1996) · 2024Article
- Methamphetamine Increases Tubulo-Vesicular Areas While Dissipating Proteins from Vesicles Involved in Cell Clearance.International journal of molecular sciences · 2024Article
- Is There a Place for Lewy Bodies before and beyond Alpha-Synuclein Accumulation? Provocative Issues in Need of Solid Explanations.International journal of molecular sciences · 2024Review
- A familial missense variant in the Alzheimer's disease gene SORL1 impairs its maturation and endosomal sorting.Acta neuropathologica · 2024Article
- Analysis of the neuromuscular deficits caused by STAM1 deficiency.Current research in neurobiology · 2024Article
- A familial missense variant in the Alzheimer's Disease genebioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a chronic neurodegenerative disease that is characterized by a loss of dopaminergic neurons in the substantia nigra pars compacta of the midbrain (SNpc). Extensive studies into genetic and cellular models of PD implicate protein trafficking as a prominent contributor to the death of these dopaminergic neurons. Considerable evidence also suggests the involvement of α-synuclein as a central component of the characteristic cell death in PD and it is a major structural constituent of proteinaceous inclusion bodies (Lewy bodies; LB). α-synuclein research has been a vital part of PD research in recent years, with newly discovered evidence suggesting that α-synuclein can propagate through the brain via prion-like mechanisms. Healthy cells can internalize toxic α-synuclein species and seed endogenous α-synuclein to form large, pathogenic aggregates and form LBs. A better understanding of how α-synuclein can propagate, enter and be cleared from the cell is vital for therapeutic strategies.
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