ReviewMetabolic brain disease2026
The role of 2-Oxoglutarate dehydrogenase complex mitochondrial enzyme in alzheimer's disease: a literature review and bioinformatics workflow.
Review in Metabolic brain disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
10 authors.
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Abstract
Alzheimer’s disease (AD) is a leading neurodegenerative disorder and a significant cause of senile dementia. While the exact mechanisms of AD remain unclear, key hypotheses include the accumulation of amyloid-β (Aβ) plaques and hyperphosphorylated Tau tangles in the hippocampus and cortex. Recent evidence highlights the significant role of damaged mitochondria in AD pathogenesis. Abnormal glucose metabolism contributes to neurodegeneration by affecting enzymes in the tricarboxylic acid (TCA) cycle, particularly the mitochondrial 2-oxoglutarate dehydrogenase (OGDHC) complex, which is vital for the oxidative decarboxylation of 2-oxoglutarate. Impaired OGDHC function is associated with energy failure, oxidative stress, neuroinflammation, and calcium irregularities, all of which may worsen AD progression. This study reviews the evidence linking mitochondrial dysfunction to AD, emphasizing OGDHC deficiency. Additionally, we conducted a bioinformatics analysis to identify key genes in mitochondrial metabolic pathways, highlighting the critical role of OGDHC in AD-related mitochondrial dysfunction (Graphical abstract = Fig. 2).
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41945181What Socratic 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 Socratic graph.