ReviewMolecular neurobiology2013
α-Synuclein elevation in human neurodegenerative diseases: experimental, pathogenetic, and therapeutic implications.
Review in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
- Gene delivery of SUMO1-derived peptide rescues neuronal degeneration and motor deficits in a mouse model of Parkinson's disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The Effects of Air Pollution on Neurological Diseases: A Narrative Review on Causes and Mechanisms.Toxics · 2025Review
- A clinical study and future prospects for bioactive compounds and semi-synthetic molecules in the therapies for Huntington's disease.Molecular neurobiology · 2024Review
- Overexpression-Induced α-Synuclein Brain Spreading.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- A comprehensive understanding of ambient particulate matter and its components on the adverse health effects based from epidemiological and laboratory evidence.Particle and fibre toxicology · 2022Review
- Traumatic brain injury and the development of parkinsonism: Understanding pathophysiology, animal models, and therapeutic targets.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Review
- Exploration in the Therapeutic and Multi-Target Mechanism of Ketamine on Cerebral Ischemia Based on Network Pharmacology and Molecular Docking.International journal of general medicine · 2022Article
- Refinement of α-Synuclein Ensembles Against SAXS Data: Comparison of Force Fields and Methods.Frontiers in molecular biosciences · 2021Article
- Absence of Glia Maturation Factor Protects from Axonal Injury and Motor Behavioral Impairments after Traumatic Brain Injury.Experimental neurobiology · 2020Article
- Impact of α-synuclein pathology on transplanted hESC-derived dopaminergic neurons in a humanized α-synuclein rat model of PD.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Effects of air pollution on the nervous system and its possible role in neurodevelopmental and neurodegenerative disorders.Pharmacology & therapeutics · 2020Review
- Overexpression of human wtTDP-43 causes impairment in hippocampal plasticity and behavioral deficits in CAMKII-tTa transgenic mouse model.Molecular and cellular neurosciences · 2020Article
- A30P mutant α-synuclein impairs autophagic flux by inactivating JNK signaling to enhance ZKSCAN3 activity in midbrain dopaminergic neurons.Cell death & disease · 2019Article
- Long-lasting pathological consequences of overexpression-induced α-synuclein spreading in the rat brain.Aging cell · 2018Article
- Transmission of α-synuclein-containing erythrocyte-derived extracellular vesicles across the blood-brain barrier via adsorptive mediated transcytosis: another mechanism for initiation and progression of Parkinson's disease?Acta neuropathologica communications · 2017Article
- Cystatin C as a potential therapeutic mediator against Parkinson's disease via VEGF-induced angiogenesis and enhanced neuronal autophagy in neurovascular units.Cell death & disease · 2017Article
- The Contribution ofNeural plasticity · 2017Review
- The Chemical Molecule B355252 is Neuroprotective in an In Vitro Model of Parkinson's Disease.Cellular and molecular neurobiology · 2016Article
- Preparation and Characterization of Stable α-Synuclein Lipoprotein Particles.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The discovery of α-synuclein has had profound implications concerning our understanding of Parkinson's disease (PD) and other neurodegenerative disorders characterized by α-synuclein accumulation. In fact, as compared with pre-α-synuclein times, a "new" PD can now be described as a whole-body disease in which a progressive spreading of α-synuclein pathology underlies a wide spectrum of motor as well as nonmotor clinical manifestations. Not only is α-synuclein accumulation a pathological hallmark of human α-synucleinopathies but increased protein levels are sufficient to trigger neurodegenerative processes. α-Synuclein elevations could also be a mechanism by which disease risk factors (e.g., aging) increase neuronal vulnerability to degeneration. An important corollary to the role of enhanced α-synuclein in PD pathogenesis is the possibility of developing α-synuclein-based biomarkers and new therapeutics aimed at suppressing α-synuclein expression. The use of in vitro and in vivo experimental models, including transgenic mice overexpressing α-synuclein and animals with viral vector-mediated α-synuclein transduction, has helped clarify pathogenetic mechanisms and therapeutic strategies involving α-synuclein. These models are not devoid of significant limitations, however. Therefore, further pursuit of new clues on the cause and treatment of PD in this post-α-synuclein era would benefit substantially from the development of improved research paradigms of α-synuclein elevation.
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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.