ReviewTrends in neurosciences2009
Calcium homeostasis, selective vulnerability and Parkinson's disease.
Review in Trends in neurosciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
112 citing papers in PubMed, 1 synthesis or guideline pooled it, 236 citations in OpenAlex.
- Identifying consensus disease pathways in Parkinson's disease using an integrative systems biology approach.PloS one · 2011Pooled it
- The human LRRK2-R1441G mutation drives age-dependent oxidative stress and mitochondrial dysfunction in dopaminergic neurons.Molecular neurodegeneration · 2026Article
- Zebrafish Models of Parkinson's Disease: From Pathogenesis to Drug Discovery.International journal of molecular sciences · 2026Review
- Nanoscale CabioRxiv : the preprint server for biology · 2026Article
- Stem Cell-Derived Exosomes Regulate Mitochondrial Function: A Novel Strategy for Parkinson's Disease Therapy.Molecular neurobiology · 2026Review
- Role of STX1A in Parkinson's disease: evidence, mechanistic hypotheses, and translational perspectives.Frontiers in aging neuroscience · 2026Review
- Mitochondrial and lysosomal dysfunctions might be involved in the pathogenesis of the CACNA1A-related neurodevelopmental disorders according to in vitro studies.Biological research · 2025Article
- Targeting Cdc42 improves motor phenotype in Parkinson's disease mice and reveals age-dependent susceptibility to α-synuclein.iScience · 2025Article
- The Human LRRK2-R1441G Mutation Drives Age-Dependent Oxidative Stress and Mitochondrial Dysfunction in Dopaminergic Neurons.Research square · 2025Article
- Dysfunction of subthalamic dopaminergic circuitry contributes to anxiety- and depression-like behaviors in 6-OHDA lesion-induced hemiparkinsonian mice.Acta pharmacologica Sinica · 2025Article
- The neuroprotective effects of nanocurcumin on Parkinson's disease markers in rats exposed to tin chloride.3 Biotech · 2025Article
- Imaging advances to detect non-motor prodromal markers of Parkinson's disease and explore therapeutic translation opportunities.NPJ Parkinson's disease · 2025Review
- Molecular signatures of regional vulnerability to tauopathy in excitatory cortical neurons.Acta neuropathologica · 2025Article
- Caloric Restriction Mimetics as Priming Agents of Mesenchymal Stem Cells Secretome to Enhance Regenerative Responses to Parkinson's Disease.Molecules (Basel, Switzerland) · 2025Review
- PD-linked LRRK2 G2019S mutation impairs astrocyte morphology and synapse maintenance via ERM hyperphosphorylation.bioRxiv : the preprint server for biology · 2025Article
- Distinct cortical morphometric inverse divergence changes in Parkinson's disease correlate with transcriptional expression patterns.NeuroImage. Clinical · 2025Article
- Transcriptional expression patterns of the cortical morphometric similarity network in progressive supranuclear palsy.CNS neuroscience & therapeutics · 2024Article
- Morphometric similarity differences in drug-naive Parkinson's disease correlate with transcriptomic signatures.CNS neuroscience & therapeutics · 2024Article
- NPC1-dependent alterations in KNature communications · 2023Article
- Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Parkinson's disease (PD) is a common neurodegenerative disorder of which the core motor symptoms are attributable to the degeneration of dopamine (DA) neurons in the substantia nigra pars compacta (SNc). Recent work has revealed that the engagement of L-type Ca(2+) channels during autonomous pacemaking renders SNc DA neurons susceptible to mitochondrial toxins used to create animal models of PD, indicating that homeostatic Ca(2+) stress could be a determinant of their selective vulnerability. This view is buttressed by the central role of mitochondria and the endoplasmic reticulum (linchpins of current theories about the origins of PD) in Ca(2+) homeostasis. Here, we summarize this evidence and suggest the dual roles had by these organelles could compromise their function, leading to accelerated aging of SNc DA neurons, particularly in the face of genetic or environmental stress. We conclude with a discussion of potential therapeutic strategies for slowing the progression of PD.
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What OpenQuestion holds
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.