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In addition to the inadequate availability of glucose for use by neurons, the mitochondrial dysfunction and dysregulated glycolysis that occur in AD inhibit oxidative phosphorylation and result in decreased tricarboxylic acid substrates required for the synthesis of neurotransmitters, such as GABA and acetylcholine, further contributing to the pathology of this disease [58, 60, 61]

Wang R, Samudio IJ, McQueen T, Schober WD, Ruvolo VR, Kornblau SM, Konopleva M, Andreeff

In a diabetic mouse model, it reduced oxidative stress-induced neuropathy by triggering antioxidative defense signals (Agca et al

however, its limited specificity fails to discriminate IBD from other inflammatory or infectious conditions, and unchanged levels in a subset of patients restrict its accuracy for assessing disease activity [556, 557]