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Reductions of CMR glc commonly are correlated with cognitive decline in patients with AD, in particular in the parietotemporal, frontal, and posterior cingulate cortices ( 18 F]FDG reveals the progressive reduction in cerebral glucose metabolism in patients with subsequent pathologically proven AD before clinical symptoms are detected ( In the precuneus and parietal, temporal, and occipital cortices, and in cerebellum, participants treated with placebo had significantly decreased CMR glc after 6 months, in agreement with PET determinations of glucose metabolism in AD that show a consistent pattern of reduced cerebral glucose utilization beginning in parietal and temporal regions, later spreading to prefrontal cortices ( glc decrease is compatible with previous reports ( 18 F]FDG metabolite retention in brain is sensitive to disease progression, and decline is closely related to cognitive impairment ( glc after 6 months, implying that the GLP-1 analog treatment prevented the decline of CMR glc that reflects cognitive impairment, synaptic dysfunction, and disease progression, despite longer disease duration in this group