Publications by authors named "Yuliya D Smirnova"
Article Synopsis
- Mitochondrial dysfunction and glutamate toxicity are linked to neural disorders, particularly brain trauma, and involve two separate pathways: a transmission pathway (via synaptic GluN2A receptors) and a toxic pathway (via extrasynaptic GluN2B receptors).
- The toxic pathway is exacerbated by neuro-inflammation, leading to the inhibition of the 2-oxoglutarate dehydrogenase complex (OGDHC), which increases extracellular glutamate levels and contributes to cell damage.
- Therapies targeting the tricarboxylic acid (TCA) cycle may be more effective for treating neurological disorders than those focusing solely on preserving mitochondrial function.
Mitochondrial dysfunction in the ischemic brain is one of the hallmarks of stroke. Dietary interventions such as the ketogenic diet and hydroxycitric acid supplementation (a caloric restriction mimetic) may potentially protect neurons from mitochondrial damage induced by focal stroke in mice. We showed that in control mice, the ketogenic diet and the hydroxycitric acid did not impact significantly on the mtDNA integrity and expression of genes involved in the maintenance of mitochondrial quality control in the brain, liver, and kidney.
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