ReviewMolecular neurodegeneration2017
Post translational changes to α-synuclein control iron and dopamine trafficking; a concept for neuron vulnerability in Parkinson's disease.
Review in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 73 citations in OpenAlex.
- From synaptic development to degeneration: a narrative review of small molecule strategies targeting alpha-synuclein in Parkinson's disease.Metabolic brain disease · 2026Review
- Plant natural products targeting NLRP3 inflammasome in Parkinson's disease: Molecular activation and regulation to therapeutics.iScience · 2026Review
- Periodic limb movements in Parkinson's disease: a critical review of pathophysiology and a framework for clinical management.NPJ Parkinson's disease · 2026Review
- Ferroptosis inhibition protects against α-synuclein-related neuronal cell death.Cell death & disease · 2025Article
- Surface wetting is a key determinant of α-synuclein condensate maturation.Communications chemistry · 2025Article
- Mesenchymal stem cell-derived exosomes as a potential therapeutic strategy for ferroptosis.Stem cell research & therapy · 2025Review
- Levodopa-induced dyskinesia: brain iron deposition as a new hypothesis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
- Tau accumulation is associated with dopamine deficiency in vivo in four-repeat tauopathies.European journal of nuclear medicine and molecular imaging · 2024Article
- Review
- Glial cells improve Parkinson's disease by modulating neuronal function and regulating neuronal ferroptosis.Frontiers in cell and developmental biology · 2024Review
- Diosgenin derivative ML5 attenuates MPTP-induced neuronal impairment via regulating AMPK/PGC-1α-mediated mitochondrial biogenesis and fusion/fission.American journal of translational research · 2024Article
- Protein kinase R dependent phosphorylation of α-synuclein regulates its membrane binding and aggregation.PNAS nexus · 2022Article
- Oxidative Stress as a Potential Mechanism Underlying Membrane Hyperexcitability in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Keeping Cell Death Alive: An Introduction into the French Cell Death Research Network.Biomolecules · 2022Review
- A Facile Method to Produce N-Terminally Truncated α-Synuclein.Frontiers in neuroscience · 2022Article
- Extracellular α-Synuclein Modulates Iron Metabolism Related Proteins via Endoplasmic Reticulum Stress in MES23.5 Dopaminergic Cells.Neurochemical research · 2021Article
- Enhancing Top-Down Proteomics of Brain Tissue with FAIMS.Journal of proteome research · 2021Article
- Cholinergic Receptor Modulation as a Target for Preventing Dementia in Parkinson's Disease.Frontiers in neuroscience · 2021Review
- Ferroptosis as a New Mechanism in Parkinson's Disease Therapy Using Traditional Chinese Medicine.Frontiers in pharmacology · 2021Review
- Parkinson's Disease Dementia: Synergistic Effects of Alpha-Synuclein, Tau, Beta-Amyloid, and Iron.Frontiers in aging neuroscience · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Parkinson's disease is a multifactorial neurodegenerative disorder, the aetiology of which remains elusive. The primary clinical feature of progressively impaired motor control is caused by a loss of midbrain substantia nigra dopamine neurons that have a high α-synuclein (α-syn) and iron content. α-Syn is a neuronal protein that is highly modified post-translationally and central to the Lewy body neuropathology of the disease. This review provides an overview of findings on the role post translational modifications to α-syn have in membrane binding and intracellular vesicle trafficking. Furthermore, we propose a concept in which acetylation and phosphorylation of α-syn modulate endocytic import of iron and vesicle transport of dopamine during normal physiology. Disregulated phosphorylation and oxidation of α-syn mediate iron and dopamine dependent oxidative stress through impaired cellular location and increase propensity for α-syn aggregation. The proposition highlights a connection between α-syn, iron and dopamine, three pathological components associated with disease progression in sporadic 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.