ReviewThe Journal of biological chemistry2013
Calcium, bioenergetics, and neuronal vulnerability in Parkinson's disease.
Review in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 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.
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Who cites it
113 citing papers in PubMed.
- Correlative ultrastructural mapping of Lewy pathology reveals regional diversity in Parkinson's and dementia with Lewy bodies.Acta neuropathologica · 2026Article
- Nicotinamide Riboside Enhances Mitochondrial Bioenergetics and Dopaminergic Signaling Independent of Neuron Survival in a Double-Hit Parkinson's Model.Research square · 2026Article
- Nanoscale CabioRxiv : the preprint server for biology · 2026Article
- α-Synuclein oligomers slow down action potential firing and enhance dopamine release by increasing Cav2.2 currents in midbrain dopaminergic neurons.The Journal of physiology · 2026Article
- Autophagy-lysosomal pathway in neurodegeneration.Molecular neurodegeneration advances · 2026Review
- Creatine-weighted imaging in patients with Parkinson's disease.NPJ Parkinson's disease · 2025Article
- 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
- Disease-modifying, multidimensional efficacy of putaminal CaMolecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Chronic hyperactivation of midbrain dopamine neurons causes preferential dopamine neuron degeneration.eLife · 2025Article
- Comparative mapping of single-cell transcriptomic landscapes in neurodegenerative diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Comparative mapping of single-cell transcriptomic landscapes in neurodegenerative diseases.bioRxiv : the preprint server for biology · 2024Article
- Advancements in Targeting Ion Channels for the Treatment of Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Selective dopaminergic neurotoxicity modulated by inherent cell-type specific neurobiology.Neurotoxicology · 2024Review
- Neurovascular and immune factors of vulnerability of substantia nigra dopaminergic neurons in non-human primates.NPJ Parkinson's disease · 2024Article
- From Synaptic Physiology to Synaptic Pathology: The Enigma of α-Synuclein.International journal of molecular sciences · 2024Review
- Calcium Modulating Effect of Polycyclic Cages: A Suitable Therapeutic Approach Against Excitotoxic-induced Neurodegeneration.Mini reviews in medicinal chemistry · 2024Review
- Prevention of Parkinson's Disease: From Risk Factors to Early Interventions.CNS & neurological disorders drug targets · 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
- Review
- 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
53 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The most distinguishing feature of neurons is their capacity for regenerative electrical activity. This activity imposes a significant mitochondrial burden, especially in neurons that are autonomously active, have broad action potentials, and exhibit prominent Ca(2+) entry. Many of the genetic mutations and toxins associated with Parkinson's disease compromise mitochondrial function, providing a mechanistic explanation for the pattern of neuronal pathology in this disease. Because much of the neuronal mitochondrial burden can be traced to L-type voltage-dependent channels (channels for which there are brain-penetrant antagonists approved for human use), a neuroprotective strategy to reduce this burden is available.
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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.