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A broad number of studies have demonstrated the reduction of glucose uptake in the brain of AD patients, and, in agreement, positron emission tomography (PET) scanning shows a consistent reduction of cerebral glucose consumption in the brain of AD patients (390, 391)

Animal studies have shown that the selective small-molecule inhibitor 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO), targeting the key glycolytic enzyme Phosphofructokinase-2/fructose-2,6-bisphosphatase 3 (PFKFB3), disrupts T cell metabolism, culminating in reduced cell proliferation and heightened cell death rates

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doi: 10.1111/epi.13060