ReviewBrain research bulletin2017
Metabolic Dysfunction in Parkinson's Disease: Bioenergetics, Redox Homeostasis and Central Carbon Metabolism.
Review in Brain research bulletin, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 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
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
99 citing papers in PubMed, 163 citations in OpenAlex.
- The SLC7A11 Thermostat: A Molecular Signaling Switch Between Ferroptosis and Disulfidptosis in Neurodegenerative Disease.Molecular neurobiology · 2026Review
- Proteo-metabolomic integration identifies stage-specific candidate biomarkers for Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Proteoform-Resolved Cross-Linking Reveals Environment-Dependent Structural Effects of α-Synuclein S129 Phosphorylation.Journal of the American Chemical Society · 2026Article
- Mitochondria-Targeted Nanotherapies in Aging Neurodegenerative Disorders: Emerging Prospects and Clinical Potential.Advanced healthcare materials · 2026Review
- Chlorogenic Acid Fails to Confer Neuroprotection in a Chronic Mouse Model of Parkinson's Disease.Molecular neurobiology · 2026Article
- BjPro-7a, A Proline-Rich Peptide from Bothrops jararaca Venom, Reverses MPP⁺-Induced Locomotor Deficits and Rescues Mitochondrial, Redox, and Synaptic Proteomic Pathways in a Zebrafish Model of Parkinsonism.Neurochemical research · 2026Article
- Spatial multi-omics reveals region-specific molecular signatures in a 6-OHDA model of Parkinson's disease.NPJ Parkinson's disease · 2026Article
- DJ-1 in the Neuro-cutaneous Aging Axis: Unifying Pathways of Parkinson's Disease Neurodegeneration, Progression, and Redox-Based Therapeutic Strategies for Healthy Longevity.Molecular neurobiology · 2026Review
- Early GPR81/MCT1 rise and late lactate-NAD(H) Build-up in an LPS model of PD.Metabolic brain disease · 2026Article
- Longitudinal Repeatome Remodeling in Peripheral Blood Following Parkinson's Disease Diagnosis.Genes · 2026Article
- Parkinson's Disease: From Metabolism to Genetics-A Comprehensive Review.Current issues in molecular biology · 2026Review
- Gastrodin inhibits hexokinase-2 mediated glycolysis to rescue rotenone-damaged PC12 cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Transaldolase 1 impacts Parkinson's disease pathogenesis via metabolic reprogramming and autophagy-lysosomal pathway.Acta neuropathologica communications · 2025Article
- Dysfunctional digestive tract highlights the metabolic hallmarks of nanoplastic-exacerbated Parkinson's pathology.NPJ Parkinson's disease · 2025Article
- Sex-dependent effects of a high-fat diet-induced obesity model on cerebrovascular health and brain metabolism.Experimental physiology · 2025Article
- A rationally designed microbial consortium modulates neurodegeneration in a Drosophila melanogaster model of Parkinson's disease.NPJ biofilms and microbiomes · 2025Article
- Exploring the Causal Links Between 338 Cerebrospinal Fluid Metabolites and Parkinson's Disease.Brain and behavior · 2025Article
- Mitochondrial Energy Transformation Capacity Influences Brain Activation During Sensory, Affective, and Cognitive Tasks.bioRxiv : the preprint server for biology · 2025Article
- Exploring the mechanism of metabolic cell death-related genes AKR1C2 and MAP1LC3A as biomarkers in Parkinson's disease.Scientific reports · 2025Article
- Exercise Ameliorates Dysregulated Mitochondrial Fission, Mitochondrial Respiration, and Neuronal Apoptosis in Parkinson's Disease Mice via the Irisin/AMPK/SIRT1 Pathway.Molecular neurobiology · 2025Article
39 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
8 authors at 3 institutions in 3 countries.
Funding
Abstract
The loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the accumulation of protein inclusions (Lewy bodies) are the pathological hallmarks of Parkinson's disease (PD). PD is triggered by genetic alterations, environmental/occupational exposures and aging. However, the exact molecular mechanisms linking these PD risk factors to neuronal dysfunction are still unclear. Alterations in redox homeostasis and bioenergetics (energy failure) are thought to be central components of neurodegeneration that contribute to the impairment of important homeostatic processes in dopaminergic cells such as protein quality control mechanisms, neurotransmitter release/metabolism, axonal transport of vesicles and cell survival. Importantly, both bioenergetics and redox homeostasis are coupled to neuro-glial central carbon metabolism. We and others have recently established a link between the alterations in central carbon metabolism induced by PD risk factors, redox homeostasis and bioenergetics and their contribution to the survival/death of dopaminergic cells. In this review, we focus on the link between metabolic dysfunction, energy failure and redox imbalance in PD, making an emphasis in the contribution of central carbon (glucose) metabolism. The evidence summarized here strongly supports the consideration of PD as a disorder of cell metabolism.
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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.