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In order to test this possibility, we engineered a murinized version of the anti-IGF-1R mAb, L2-C (L2-Cmu), in order to reduce effector function and enable chronic administration in mice

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The PI3K/Akt pathway activated by IGF1R is a major anti-apoptotic pathway in neurons, which drives interest in IGF1R agonism as a potential neuroprotective strategy in preclinical research