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Brain energy metabolism spurns fatty acids as fuel due to their inherent mitotoxicity and potential capacity to unleash neurodegeneration

Additionally, it demonstrated the differential expression of oxidative stress-related genes, such as SOD1, induced by ketamine ( A study using immunofluorescent staining confirmed that ketamine treatment resulted in increased expression levels of glucose transporter 3 (GLUT3) and phosphorylated ERK1/2 (P-ERK1/2) in astrocytes, but not in neurons, within the prefrontal cortex and suggested that ketamine enhances glucose metabolism in the prefrontal cortex through the nuclear localization of P-ERK1/2 in astrocytes, which promotes the expression of GLUT3 ( Immunofluorescence staining of a human microglial cell line shows the nuclear translocation of the signal transducer and activation of transcription 3 (STAT3) after the cells were treated with ketamine

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Across multiple experimental modelsincluding Parkinsons disease, Alzheimers disease, and cerebral ischemia-reperfusion injuryriboflavin supplementation has demonstrated consistent neuroprotective effects, reflected in reduced oxidative burden and preservation of neuronal integrity (34)