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Hippocampal glucose metabolism refers to the collective pathways by which glucose is taken up, processed, and utilized by cells in the hippocampus, a critical brain region for memory and cognition. This process involves glucose transporters (such as GLUTs), glycolysis, oxidative phosphorylation, and astrocyte-neuron lactate shuttling, among other mechanisms. Hippocampal glucose metabolism is altered in various brain disorders, including Alzheimer’s disease (where microglia and astrocytes show characteristic metabolic changes)[1][2][4], psychosis[5], and normal aging[3]. Deficits in this process are associated with neuronal dysfunction, atrophy of hippocampal subfields, and cognitive impairment. Some experimental drugs act indirectly to modify hippocampal glucose metabolism by targeting upstream metabolic regulators, such as the enzyme IDO1 in glial cells[2][4]. This entry is not a molecular drug target or receptor, but a tissue-level metabolic phenotype/process. For specific targets, such as glucose transporters (GLUTs), metabolic enzymes (e.g., hexokinase, pyruvate dehydrogenase), or regulators (e.g., IDO1), please specify the molecule of interest.
IDO1 inhibition restores astrocyte-derived glycolytic support (lactate production/transfer) to neurons, normalizing glucose metabolism in the hippocampus[2][4].
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