ArticleNature communications2023
A reversible state of hypometabolism in a human cellular model of sporadic Parkinson's disease.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Differential effects of hormone therapy formulations on Parkinson's disease risk: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Pooled it
- Transcriptional and epigenetic regulation of autophagy: mechanisms, disease relevance and therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Research progress on the Sonic Hedgehog signaling pathway in the central nervous system: Novel insights.Neural regeneration research · 2026Article
- TNF alpha unmasks enteric malate aspartate shuttle dysfunction bridging Parkinson disease and intestinal inflammation.Nature communications · 2026Article
- Article
- Metabolomics of Multiple System Atrophy Patient-Derived Striatal Medium Spiny Neurons.Biomolecules · 2026Article
- Glycerol 3-phosphate acyltransferase exacerbates α-synuclein-induced toxicity by increasing lipid peroxidation.Nature communications · 2026Article
- A Distributed Oscillatory Network Model of Parkinsonian Tremor: Integrating Basal Ganglia and Cerebello-Thalamic Circuits.Tremor and other hyperkinetic movements (New York, N.Y.) · 2026Review
- Temporin-1CEa and its Analog LK2(6)A(L) Confer Neuroprotective Effects in Parkinson's Disease Model by Attenuating Neuroinflammation Via the NF-κB and MAPK Signaling Pathways.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Inkjet-Printed 3D Sensor Arrays with FIB-Induced Electrode Refinement for Low-Noise Amperometric Recordings in hiPSC-Derived Brain Organoids.ACS sensors · 2025Article
- Human Glucose Transporters in Health and Selected Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Mitochondrial dysfunction-mediated metabolic remodeling of TCA cycle promotes Parkinson's disease through inhibition of H3K4me3 demethylation.Cell death discovery · 2025Article
- Analysis of dopaminergic neuron-specific mitochondrial morphology and function using tyrosine hydroxylase reporter iPSC lines.Anatomical science international · 2025Review
- Dysregulation of mitochondrial α-ketoglutarate dehydrogenase leads to elevated lipid peroxidation in CHCHD2-linked Parkinson's disease models.Nature communications · 2025Article
- Parkinson's disease physiopathology-beyond theFrontiers in aging neuroscience · 2025Review
- Proteomic insights into the biology of dopaminergic neurons.Frontiers in molecular neuroscience · 2025Review
- Dopaminergic neuron metabolism: relevance for understanding Parkinson's disease.Metabolomics : Official journal of the Metabolomic Society · 2024Review
- Glycolytic metabolism: Food for immune cells, fuel for depression?Brain, behavior, & immunity - health · 2024Article
- Histone post-translational modification and heterochromatin alterations in neurodegeneration: revealing novel disease pathways and potential therapeutics.Frontiers in molecular neuroscience · 2024Review
Corrections and comments
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Authors and funding
24 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sporadic Parkinson's Disease (sPD) is a progressive neurodegenerative disorder caused by multiple genetic and environmental factors. Mitochondrial dysfunction is one contributing factor, but its role at different stages of disease progression is not fully understood. Here, we showed that neural precursor cells and dopaminergic neurons derived from induced pluripotent stem cells (hiPSCs) from sPD patients exhibited a hypometabolism. Further analysis based on transcriptomics, proteomics, and metabolomics identified the citric acid cycle, specifically the α-ketoglutarate dehydrogenase complex (OGDHC), as bottleneck in sPD metabolism. A follow-up study of the patients approximately 10 years after initial biopsy demonstrated a correlation between OGDHC activity in our cellular model and the disease progression. In addition, the alterations in cellular metabolism observed in our cellular model were restored by interfering with the enhanced SHH signal transduction in sPD. Thus, inhibiting overactive SHH signaling may have potential as neuroprotective therapy during early stages of sPD.
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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.