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These medications work by mimicking the action of naturally occurring GLP-1, an incretin hormone released by the intestine in response to food intake

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Over time, this energy shortfall sets off a cascade of downstream effects: synaptic dysfunction, impaired protein clearance, neuroinflammation, and ultimately the accumulation of amyloid- and tau pathology Importantly, imaging and metabolic studies consistently show that reductions in cerebral glucose metabolism and perfusion precede cognitive symptoms by years, often decades [8]