ArticleMovement disorders : official journal of the Movement Disorder Society2012
Living on the edge with too many mouths to feed: why dopamine neurons die.
Article in Movement disorders : official journal of the Movement Disorder Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 248 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.
The trial behind it
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Who cites it
248 citing papers in PubMed, 444 citations in OpenAlex.
- Regulation and roles of mammalian mitophagy.Nature reviews. Molecular cell biology · 2026Review
- Spatiotemporal Resolution for Neurodegenerative Diseases: Linking Proteinopathy, Cellular Vulnerability, and Disease Trajectories.Neuroscience bulletin · 2026Review
- Species-dependent activities of the PINK1-parkin axis.Translational neurodegeneration · 2026Review
- Mitochondrial Quality Control Imbalance in the Heterogeneity of Parkinson's Disease: From Selective Vulnerability to Stratified Transformation.International journal of molecular sciences · 2026Review
- Batch- and Composition-Controlled Reanalysis of Bulk and Single-Nucleus Transcriptomes Reveals Co-Enrichment of Glial Complement and of Translational Signatures in Parkinson's Disease and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Article
- When Pathologies Collide: The Intersection of Tau and Alpha-Synuclein in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Beyond phenotypic markers: rethinking dopaminergic identity in iPSC-derived neurons.Cell communication and signaling : CCS · 2026Review
- Selective Neuronal Vulnerability to Alpha-Synuclein Pathology in Parkinson's Disease: A Critical Review of Mechanistic Rationale and Biomarker Stratification.Medical sciences (Basel, Switzerland) · 2026Review
- Charting the human-specific properties of gene expression networks in the infant prefrontal cortex.Science advances · 2026Article
- Cell-based regenerative interventions in Parkinson's disease: Overcoming pharmacological limitations.Acta pharmaceutica Sinica. B · 2026Review
- Alzheimer's Pathology Enhances Excitatory Synaptic Input and Integration in VTA Dopamine Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Propagation of α-synuclein pathology: models, mechanisms and future goals.Molecular neurodegeneration advances · 2026Review
- Neuroprotective role of bilirubin in Parkinson's disease.Frontiers in aging neuroscience · 2026Review
- The Golgi apparatus: adaptations to neuronal shape and functions.The EMBO journal · 2026Review
- Mitochondrial dysfunction and oxidative stress in Parkinson's disease: mechanisms, biomarkers, and therapeutic strategies.Tissue barriers · 2026Review
- Age-related changes to brain energetics revealed by PET/MRI imaging.NeuroImage. Clinical · 2026Article
- Creatine-weighted imaging in patients with Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Buried Treasure? Overlooked and Newly Discovered Evolutionary Contributions to Human Brain Diseases.Annals of neurology · 2025Review
- Movement disorders: a brief overview from an evolutionary perspective.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Sleep deprivation and risk for Parkinson's disease: evidence and therapeutic implications.Journal of neurology · 2025Review
188 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
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Although genes, protein aggregates, environmental toxins, and other factors associated with Parkinson's disease (PD) are widely distributed in the nervous system and affect many classes of neurons, a consistent feature of PD is the exceptional and selective vulnerability of dopamine (DA) neurons of the SNc. What is it about these neurons, among all other neurons in the brain, that makes them so susceptible in PD? We hypothesize that a major contributory factor is the unique cellular architecture of SNc DA neuron axons. Their large, complex axonal arbour puts them under such a tight energy budget that it makes them particularly susceptible to factors that contribute to cell death, including unique molecular characteristics associated with SNc DA neurons and nonspecific, nervous-system-wide factors.
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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.