The DOI matches its Crossref record; 89 of the 89 references it cites were found in a registry or an index.
Synaptic, Mitochondrial, and Lysosomal Dysfunction in Parkinson’s Disease
Open accessAbstract
The discovery of genetic forms of Parkinson's disease (PD) has highlighted the importance of the autophagy/lysosomal and mitochondrial/oxidative stress pathways in disease pathogenesis. However, recently identified PD-linked genes, including DNAJC6 (auxilin), SYNJ1 (synaptojanin 1), and the PD risk gene SH3GL2 (endophilin A1), have also highlighted disruptions in synaptic vesicle endocytosis (SVE) as a significant contributor to disease pathogenesis. Additionally, the roles of other PD genes such as LRRK2, PRKN, and VPS35 in the regulation of SVE are beginning to emerge. Here we discuss the recent work on the contribution of dysfunctional SVE to midbrain dopaminergic neurons' selective vulnerability and highlight pathways that demonstrate the interplay of synaptic, mitochondrial, and lysosomal dysfunction in the pathogenesis of PD.
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“Synaptic dysfunction contributes to disease pathogenesis in PD (Nguyen et al. 2019) and may be linked to cognitive and motor dysfunction (Bereczki et al. 2017; Moran et al. 2008).”
From Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration (2022) · cites this paper as Nguyen et al. 2019
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The Role of Oxidative Stress in Parkinson's Disease
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A meta-analysis of genome-wide association studies identifies 17 new Parkinson's disease risk loci
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Mitochondria–lysosome contacts regulate mitochondrial fission via RAB7 GTP hydrolysis
Wong, Y. C., Ysselstein, D., & Krainc, D. (2018) · Nature · doi:10.1038/nature25486 · Cited by 911
Self-citationDopamine oxidation mediates mitochondrial and lysosomal dysfunction in Parkinson’s disease
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The lipid flippase ATP10B enables cellular lipid uptake under stress conditions
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Metadata
- Authors
- Nguyen, M., Wong, Y. C., Ysselstein, D., Severino, A., & Krainc, D.
- Affiliations
- Northwestern University (US)
- Corresponding author
- Krainc, Dimitri
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 2019-02
- Volume
- 42
- Issue
- 2
- Pages
- 140-149
- ISSN
- 0166-2236 (ISSN-L)
- PMC
- PMC6452863
- OpenAlex
- W2903418495
- Cited by
- 323
- References
- 89
- Citations by year
- 2026: 25 · 2025: 38 · 2024: 53 · 2023: 42 · 2022: 45 · 2021: 57 · 2020: 45 · 2019: 18
- FWCI
- 4.73
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (2T32AG020506-16, K99 NS109252, T32 NS041234, R01 NS076054, R37 NS096241)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- Parkinson's disease, synaptic vesicle endocytosis, mitochondrial dysfunction, oxidative stress, DNAJC6, auxilin, SYNJ1, SH3GL2, endophilin A1, LRRK2, Parkin, VPS35, midbrain dopaminergic neurons, selective neuronal vulnerability, risk genes
- MeSH terms
- Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Animals, Autophagy, Dopamine, Endocytosis, Humans, Lysosomes, Mitochondria, Parkinson Disease, Synaptic Vesicles, Oxidative Stress, Genetic Predisposition to Disease, alpha-Synuclein, Dopaminergic Neurons
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