ReviewFrontiers in neuroscience2016
Calcium: Alpha-Synuclein Interactions in Alpha-Synucleinopathies.
Review in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Nanoscale CabioRxiv : the preprint server for biology · 2026Article
- Molecular Interplay of Small Molecules and Calcium Ions with α-Synuclein Revealed by NMR and Molecular Dynamics Simulations.ACS chemical neuroscience · 2026Article
- Neurodegeneration Biomarkers in Epilepsy: A Critical Review of Current Findings.Life (Basel, Switzerland) · 2026Review
- Alpha-Synuclein Dynamics in Cerebral Ischemia.ASN neuro · 2026Review
- Fasudil inhibits α-synuclein aggregation through ROCK-inhibition-mediated mechanisms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Physiological and pathological effects of phase separation in the central nervous system.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Peripheral Upregulation of Parkinson's Disease-Associated Genes Encoding α-Synuclein, β-Glucocerebrosidase, and Ceramide Glucosyltransferase in Major Depression.International journal of molecular sciences · 2024Article
- Angiotensin type 1 receptor activation promotes neuronal and glial alpha-synuclein aggregation and transmission.NPJ Parkinson's disease · 2024Article
- Lipids and α-Synuclein: adding further variables to the equation.Frontiers in molecular biosciences · 2024Review
- Monomeric α-synuclein activates the plasma membrane calcium pump.The EMBO journal · 2023Article
- Insights into Neurodegeneration in Parkinson's Disease from Single-Cell and Spatial Genomics.Movement disorders : official journal of the Movement Disorder Society · 2023Article
- The roles of connectivity and neuronal phenotype in determining the pattern of α-synuclein pathology in Parkinson's disease.Neurobiology of disease · 2022Review
- Innovative treatment targeting gangliosides aimed at blocking the formation of neurotoxic α-synuclein oligomers in Parkinson's disease.Glycoconjugate journal · 2022Review
- Alpha-Synuclein species in oral mucosa as potential biomarkers for multiple system atrophy.Frontiers in aging neuroscience · 2022Article
- Ca2+ administration prevents α-synuclein proteotoxicity by stimulating calcineurin-dependent lysosomal proteolysis.PLoS genetics · 2021Article
- Promising drug targets and associated therapeutic interventions in Parkinson's disease.Neural regeneration research · 2021Review
- The relationships of vitamin D, vitamin D receptor gene polymorphisms, and vitamin D supplementation with Parkinson's disease.Translational neurodegeneration · 2020Review
- Nutraceuticals Targeting Generation and Oxidant Activity of Peroxynitrite May Aid Prevention and Control of Parkinson's Disease.International journal of molecular sciences · 2020Review
- α-Synuclein Translocates to the Nucleus to Activate Retinoic-Acid-Dependent Gene Transcription.iScience · 2020Article
- Alpha-synuclein suppresses mitochondrial protease ClpP to trigger mitochondrial oxidative damage and neurotoxicity.Acta neuropathologica · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aggregation of the pre-synaptic protein, α-synuclein (α-syn), is the key etiological factor in Parkinson's disease (PD) and other alpha-synucleinopathies, such as multiple system atrophy (MSA) and Dementia with Lewy bodies (DLB). Various triggers for pathological α-syn aggregation have been elucidated, including post-translational modifications, oxidative stress, and binding of metal ions, such as calcium. Raised neuronal calcium levels in PD may occur due to mitochondrial dysfunction and/or may relate to calcium channel dysregulation or the reduced expression of the neuronal calcium buffering protein, calbindin-D28k. Recent results on human tissue and a mouse oxidative stress model show that neuronal calbindin-D28k expression excludes α-syn inclusion bodies. Previously, cell culture model studies have shown that transient increases of intracellular free Ca(II), such as by opening of the voltage-gated plasma calcium channels, could induce cytoplasmic aggregates of α-syn. Raised intracellular free calcium and oxidative stress also act cooperatively to promote α-syn aggregation. The association between raised neuronal calcium, α-syn aggregation, oxidative stress, and neurotoxicity is reviewed in the context of neurodegenerative α-syn disease and potential mechanism-based therapies.
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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.