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A plaques, which form and deposit in different regions of the brain, are recognized as foreign material by the brain and trigger an inflammatory and immune response by activating the microglia leading to neuronal degeneration and synaptic damage (2, 30)
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The consequences of these modifications are that IGF-1 LR3 retains the pharmacological activity of IGF-1 as an agonist of the IGF-1 receptor, has very low affinity for the insulin-like growth factor-binding proteins (IGFBPs), and has improved metabolic stability resulting in approximately three times greater potency than IGF-1, with a significantly longer half-life of about 2030 hours relative to IGF-1s half-life of about 1215 hours
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