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The rationale for the ELAD study is based on proposed shared pathophysiological mechanisms between T2DM and AD, and hypothesizes a potential for GLP-1 RA to influence AD pathology through multiple mechanisms, including neuroprotection, reducing A plaque formation and neuroinflammation, with supportive evidence from mouse models and a pilot study in AD participants [15]

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Cancelas J, Gottschall J, Rugg N, Graminske S, Schott M, North A, et al