ReviewCell calcium2010
Calcium, cellular aging, and selective neuronal vulnerability in Parkinson's disease.
Review in Cell calcium, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 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
109 citing papers in PubMed, 1 synthesis or guideline pooled it, 215 citations in OpenAlex.
- Identifying consensus disease pathways in Parkinson's disease using an integrative systems biology approach.PloS one · 2011Pooled it
- Beyond phenotypic markers: rethinking dopaminergic identity in iPSC-derived neurons.Cell communication and signaling : CCS · 2026Review
- Nigrostriatal dopaminergic vulnerability in Parkinson's disease: Neuroprotective strategies.Neural regeneration research · 2026Article
- Parkinson's disease as a multi-axis systems disorder: integrating molecular pathology and circuit-level therapeutics.Cell communication and signaling : CCS · 2026Review
- Calcineurin/NFAT signaling in the temporal integration of Ca²⁺ stress in neurodegeneration.Cell death discovery · 2026Review
- Nanoscale CabioRxiv : the preprint server for biology · 2026Article
- Aberrant calcium signaling and neuronal activity in the L271H CACNA1D (Cav1.3) iPSC model of neurodevelopmental disease.Molecular psychiatry · 2026Article
- Article
- Synaptic Vesicle Disruption in Parkinson's Disease: Dual Roles of α-Synuclein and Emerging Therapeutic Targets.Brain sciences · 2025Review
- Cinnarizine, a Calcium Channel Blocker, Partially Prevents the Striatal Dopamine Decline and Loss of Nigral Dopamine Neurons in the Lactacystin-Induced Rat Model of Parkinson's Disease.International journal of molecular sciences · 2025Article
- Reduced DJ-1-F1Fo ATP synthase association correlates with midbrain dopaminergic neuron vulnerability in idiopathic Parkinson's disease.Science advances · 2025Article
- Parallel Gene Expression Changes in Ventral Midbrain Dopamine and GABA Neurons during Normal Aging.eNeuro · 2025Article
- New Multiomic Studies Shed Light on Cellular Diversity and Neuronal Susceptibility in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025Review
- Implications for the role of natural products in Parkinson disease therapy.Archives of medical science : AMS · 2025Article
- The impact ofFrontiers in aging neuroscience · 2025Article
- Comparing tonic and phasic dendritic calcium in cholinergic pedunculopontine neurons and dopaminergic substantia nigra neurons.The European journal of neuroscience · 2024Article
- Inhibition of striatal dopamine release by the L-type calcium channel inhibitor isradipine co-varies with risk factors for Parkinson's.The European journal of neuroscience · 2024Article
- Nesfatin-1: A Biomarker and Potential Therapeutic Target in Neurological Disorders.Neurochemical research · 2024Review
- Tonic Activation of NR2D-Containing NMDARs Exacerbates Dopaminergic Neuronal Loss in MPTP-Injected Parkinsonian Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Riddles in the dark: Decoding the relationship between neuromelanin and neurodegeneration in locus coeruleus neurons.Neuroscience and biobehavioral reviews · 2023Review
49 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 the second most common neurodegenerative disease in developed countries. The core motor symptoms are attributable to the degeneration of dopamine (DA) neurons in the substantia nigra pars compacta (SNc). Why these neurons, and other restricted sets of non-dopamine neuron, succumb in PD is not clear. One potential clue has come from the observation that the engagement of L-type Ca2+ channels during autonomous pacemaking elevates the sensitivity of SNc DA neurons to mitochondrial toxins used to create animal models of PD, suggesting that Ca2+ entry is a factor in their selective vulnerability. Epidemiological data also supports a linkage between L-type Ca2+ channels and the risk of developing PD. This review examines the hypothesis that the primary factor driving neurodegenerative changes in PD is the metabolic stress created by sustained Ca2+ entry, particularly in the face of genetic or environmental factors that compromise oxidative defenses or proteostatic competence.
Indexed as
Identifiers
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.