ReviewFrontiers in molecular neuroscience2014
Upstream deregulation of calcium signaling in Parkinson's disease.
Review in Frontiers in molecular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Network Analysis Identifies Disease-Specific Pathways for Parkinson's Disease.Molecular neurobiology · 2018Pooled it
- Molecular Mechanisms of Dopaminergic Neuron Degeneration in Parkinson's Disease: A Comprehensive Review.Current neuropharmacology · 2026Review
- Calcium Signalling in Neurological Disorders, with Insights from Miniature Fluorescence Microscopy.Cells · 2024Review
- Loss of mitochondrial CaCell communication and signaling : CCS · 2024Article
- Review
- Converging peripheral blood microRNA profiles in Parkinson's disease and progressive supranuclear palsy.Brain communications · 2024Article
- Eleven Crucial Pesticides Appear to Regulate Key Genes That Link MPTP Mechanism to Cause Parkinson's Disease through the Selective Degeneration of Dopamine Neurons.Brain sciences · 2023Article
- The Metabolomic Approach Reveals the Alteration in Human Serum and Cerebrospinal Fluid Composition in Parkinson's Disease Patients.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Integrating the Roles of Midbrain Dopamine Circuits in Behavior and Neuropsychiatric Disease.Biomedicines · 2021Review
- Review
- α-Synuclein Overexpression Induces Lysosomal Dysfunction and Autophagy Impairment in Human Neuroblastoma SH-SY5Y.Neurochemical research · 2020Article
- Impaired cellular bioenergetics caused by GBA1 depletion sensitizes neurons to calcium overload.Cell death and differentiation · 2020Article
- Primary Active CaCold Spring Harbor perspectives in biology · 2020Review
- Comparison of the calcium-related factors in Parkinson's disease patients with healthy individuals.Caspian journal of internal medicine · 2020Article
- Mitochondrial and calcium perturbations in rat CNS neurons induce calpain-cleavage of Parkin: Phosphatase inhibition stabilizes pSerBiochimica et biophysica acta. Molecular basis of disease · 2019Article
- ER-mitochondria signaling in Parkinson's disease.Cell death & disease · 2018Review
- Promising Metabolite Profiles in the Plasma and CSF of Early Clinical Parkinson's Disease.Frontiers in aging neuroscience · 2018Article
- Article
- The role of CaDisease models & mechanisms · 2017Review
- 14-3-3 Proteins Buffer Intracellular Calcium Sensing Receptors to Constrain Signaling.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a major health problem affecting millions of people worldwide. Recent studies provide compelling evidence that altered Ca(2) (+) homeostasis may underlie disease pathomechanism and be an inherent feature of all vulnerable neurons. The downstream effects of altered Ca(2) (+) handling in the distinct subcellular organelles for proper cellular function are beginning to be elucidated. Here, we summarize the evidence that vulnerable neurons may be exposed to homeostatic Ca(2) (+) stress which may determine their selective vulnerability, and suggest how abnormal Ca(2) (+) handling in the distinct intracellular compartments may compromise neuronal health in the context of aging, environmental, and genetic stress. Gaining a better understanding of the varied effects of Ca(2) (+) dyshomeostasis may allow novel combinatorial therapeutic strategies to slow PD progression.
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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.