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Participants were randomized to receive either 9 weeks of semaglutide or placebo

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Arachidonic acid and related methyl ester mediate protein kinase C activation in intact platelets through the arachidonate metabolism pathways

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Together, these limitations reveal a fundamental weakness in the translational pipeline: Preclinical models, often biologically reductionist and poorly representative of human pathology, remain inadequate to support the development of interventions with reproducible and clinically relevant neuroprotective effects