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As previously noted, oxidative stress plays a decisive role in the pathophysiology of IBD, leading to cellular and molecular damage in various components such as membrane lipids, proteins, and deoxyribonucleic acid (DNA) in mitochondria and nuclei, ultimately resulting in tissue injury (Tian et al., 2017

Inhibition of glycolytic enzymes such as hexokinase-2 or pyruvate kinase M2 reduces lactate production, prevents neuronal apoptosis, and improves motor function, demonstrating a causal link between lactate accumulation and PD progression (Li et al., 2022

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