ReviewMolecular neurobiology2005
The alpha-ketoglutarate-dehydrogenase complex: a mediator between mitochondria and oxidative stress in neurodegeneration.
Review in Molecular neurobiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
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Who cites it
84 citing papers in PubMed, 174 citations in OpenAlex.
- DLST-driven metabolic alterations link skin to blood glucose: A translational study from mouse to human.Molecular metabolism · 2026Article
- Turnera diffusa polysaccharides promote healthy aging through conserved stress response regulation and metabolic remodeling across multiple aging models.Biogerontology · 2026Article
- A Lipoylation-PDH-TCA Transcriptional Deficit in the Alzheimer's Disease Cortex - Donor-level Multi-cohort Evidence with Neuronal-composition, Disease-specificity and Matched-null Controls.Journal of molecular neuroscience : MN · 2026Article
- Ethylmalonic and Methylsuccinic Acids Disrupt Bioenergetics and Induce Mitochondrial Permeability Transition Through Thiol Redox Modulation in Rat Striatum: Potential Mechanisms Involved in Ethylmalonic Encephalopathy.Neurochemical research · 2026Article
- An Emerging Role for OGDHL: From Mitochondrial Energy Metabolism to Neurodevelopmental Disorders.Biology · 2025Review
- Aberrant S-nitrosylation in the TCA cycle contributes to mitochondrial dysfunction, energy compromise, and synapse loss in neurodegenerative diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- A lncRNA-mediated metabolic rewiring of cell senescence.Cell reports · 2025Article
- Mitochondrial dysfunction in the regulation of aging and aging-related diseases.Cell communication and signaling : CCS · 2025Review
- Molecular architecture of the mammalian 2-oxoglutarate dehydrogenase complex.Nature communications · 2024Article
- Parapyruvate Induces Neurodegeneration in C57BL/6JNarl Mice via Inhibition of the α-Ketoglutarate Dehydrogenase Complex.ACS omega · 2024Article
- Benfotiamine Supplementation Increases Thiamine in Muscle of Endurance-Trained Mice and Affects the Energy Metabolism.Journal of nutrition and metabolism · 2024Article
- A Triterpenoid Lupeol as an Antioxidant and Anti-Neuroinflammatory Agent: Impacts on Oxidative Stress in Alzheimer's Disease.Nutrients · 2023Review
- Thiamine-Mediated Microbial Interaction between Auxotrophic Rhodococcus ruber ZM07 and Prototrophic Cooperators in the Tetrahydrofuran-Degrading Microbial Community H-1.Microbiology spectrum · 2023Article
- Paclitaxel Induces Neurotoxicity by Disrupting Tricarboxylic Acid Cycle Metabolic Balance in the Mouse Hippocampus.Journal of toxicology · 2023Article
- Thiamine deficiency in pregnancy and lactation: implications and present perspectives.Frontiers in nutrition · 2023Review
- Misfolded protein oligomers induce an increase of intracellular CaCellular and molecular life sciences : CMLS · 2022Article
- Co-expression network analysis of human tau-transgenic mice reveals protein modules associated with tau-induced pathologies.iScience · 2022Article
- B vitamin supply in plants and humans: the importance of vitamer homeostasis.The Plant journal : for cell and molecular biology · 2022Review
- Reverse and Forward Electron Flow-Induced HAntioxidants (Basel, Switzerland) · 2022Article
- Increasing Inhibition of the Rat Brain 2-Oxoglutarate Dehydrogenase Decreases Glutathione Redox State, Elevating Anxiety and Perturbing Stress Adaptation.Pharmaceuticals (Basel, Switzerland) · 2022Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Damage from oxidative stress and mitochondrial dysfunction occur together in many common neurodegenerative diseases. The enzymes that form the mitochondrial alpha-ketoglutarate- dehydrogenase complex (KGDHC), a key and arguably rate-limiting enzyme system of the tricarboxylic acid cycle, might mediate the interaction of these processes. KGDHC activity is reduced in numerous age-related neurodegenerative diseases and is diminished by oxidative stress. In Alzheimer's disease (AD), the reduction correlates highly to diminished mental performance. Thus, research has focused on the mechanisms by which select oxidants reduce KGDHC and the consequences of such a reduction. Diminished KGDHC in cells is associated with apoptosis without changes in the mitochondrial membrane potential. Studies of isolated mitochondria and of animal models suggest that a reduction in KGDHC can predispose to damage by other toxins that promote neurodegeneration. Diminished oxidative metabolism can be plausibly linked to pathological features of neurodegenerative diseases (e.g., reduced mental function, the plaques and tangles in AD). Thus, reductions in KGDHC might be central to the pathophysiology of these diseases. Studies of proteins, cells, animal models, and humans suggest that treatments to diminish, or bypass, the reduction in KGDHC might be beneficial in age-related neurodegenerative disorders.
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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.