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The implications are significant: these results raise the possibility that semaglutide may have insufficient central target engagement at the doses used, that the pharmacodynamic effect on AD-relevant pathways may be inadequate, or that targeting metabolic and inflammatory pathways may represent a fundamental limitation when applied to established amyloid-driven Alzheimers disease

[1] This inhibitory action contributes to glycines calming and reflex-modulating effects on the spinal cord-for example, helping regulate motor-neuron activity and muscle tone

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