ArticleNeurobiology of aging2014
Dysregulation of glucose metabolism is an early event in sporadic Parkinson's disease.
Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
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Who cites it
126 citing papers in PubMed, 251 citations in OpenAlex.
- A randomized feasibility trial of medium chain triglyceride-supplemented ketogenic diet in people with Parkinson's disease.BMC neurology · 2024Trial
- Dopaminergic nigrostriatal vulnerability in Parkinson's Disease with diabetes: evidence from severity-matched cohorts.European journal of nuclear medicine and molecular imaging · 2026Article
- A guanosine metabolism-bioenergetics intersection drives Parkinson's disease.bioRxiv : the preprint server for biology · 2026Article
- Distinct and combined interferon-ɑ/β-receptor-1 loss in neurons and astrocytes disrupt brain energy metabolism and drive Parkinsonian dementia.Journal of biomedical science · 2026Article
- Narrative Review "Dual Frontiers in Neurodegeneration: Pharmacological Synergies and Divergences in Parkinson's Disease and Type 2 Diabetes Mellitus".Cellular and molecular neurobiology · 2026Review
- Neuromodulatory control of energy reserves in dopaminergic neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Effects of aging and anti-aging dietary restriction on regulators of the [NADPH]/[NADPFree radical biology & medicine · 2025Review
- Transaldolase 1 impacts Parkinson's disease pathogenesis via metabolic reprogramming and autophagy-lysosomal pathway.Acta neuropathologica communications · 2025Article
- Metabolic Dysregulation in Parkinson's Disease: Non-Oxidative Phosphorylation and Its Role in Brain Energy Metabolism.Aging and disease · 2025Review
- A genetic driver of epileptic encephalopathy impairs gating of synaptic glycolysis.bioRxiv : the preprint server for biology · 2025Article
- Article
- Metabolic dysregulation and resistance to high-fat diet-induced weight gain in mice overexpressing human wild-type α-synuclein.NPJ Parkinson's disease · 2025Article
- Metabolomics in Parkinson's Disease and Correlation with Disease State.Metabolites · 2025Review
- Longitudinal multi-omics in alpha-synuclein Drosophila model discriminates disease- from age-associated pathologies in Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Enhancing NADPH to restore redox homeostasis and lysosomal function in G6PD-deficient microglia.Heliyon · 2025Article
- Insights into therapeutic approaches for the treatment of neurodegenerative diseases targeting metabolic syndrome.Molecular biology reports · 2025Review
- Parkinson's disease and glucose metabolism impairment.Translational neurodegeneration · 2025Review
- Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections.Open biology · 2025Review
- Exploring dopa decarboxylase as an ideal biomarker in Parkinson's disease with focus on regulatory mechanisms, cofactor influences, and metabolic implications.npj biomedical innovations · 2025Review
- Constraint-based modeling of bioenergetic differences between synaptic and non-synaptic components of dopaminergic neurons in Parkinson's disease.Frontiers in computational neuroscience · 2025Article
66 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Unlike most other cell types, neurons preferentially metabolize glucose via the pentose phosphate pathway (PPP) to maintain their antioxidant status. Inhibiting the PPP in neuronal cell models causes cell death. In rodents, inhibition of this pathway causes selective dopaminergic cell death leading to motor deficits resembling parkinsonism. Using postmortem human brain tissue, we characterized glucose metabolism via the PPP in sporadic Parkinson's disease (PD), Alzheimer's disease (AD), and controls. AD brains showed increased nicotinamide adenine dinucleotide phosphate (NADPH) production in areas affected by disease. In PD however, increased NADPH production was only seen in the affected areas of late-stage cases. Quantifying PPP NADPH-producing enzymes glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase by enzyme-linked immunosorbent assay, showed a reduction in the putamen of early-stage PD and interestingly in the cerebellum of early and late-stage PD. Importantly, there was no decrease in enzyme levels in the cortex, putamen, or cerebellum of AD. Our results suggest that down-regulation of PPP enzymes and a failure to increase antioxidant reserve is an early event in the pathogenesis of sporadic PD.
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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.