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doi: 10.1016/j.exer.2014.05.004 [DOI] [PubMed] [Google Scholar] 26.Wei L, Mo W, Lan S, et al

Insulin and insulin-like growth factors I and II (IGF-I and IGF-II) are critical for neuronal and glial growth, metabolic regulation, survival, gene expression, protein synthesis, neurotransmitter network modulation, and synaptic function.115 Cerebral insulin resistance may arise from the downregulation of insulin transport across the blood-brain barrier secondary to chronic peripheral hyperinsulinemia and systemic insulin resistance116 as well as from the loss of neuronal membrane insulin receptors induced by soluble amyloid-beta (A) oligomers.117 Impaired insulin signaling in the brain leads to increased activity of glycogen synthase kinase 3 beta, an enzyme implicated in enhanced A production and tau protein hyperphosphorylation.118 Furthermore, cerebral hyperinsulinemia is associated with diminished clearance of A peptides due to the competitive inhibition of insulin-degrading enzyme, a metalloprotease responsible for degrading both insulin and A, which preferentially binds insulin over A under hyperinsulinemic conditions.119 The neuroprotective properties of GLP-1RAs have been substantiated in vivo, supported by their ability to traverse the blood-brain barrier and the presence of GLP-1 receptors within the brain

Efficacy and safety of once-weekly semaglutide versus once-daily sitagliptin as an add-on to metformin, thiazolidinediones, or both, in patients with type 2 diabetes (SUSTAIN 2): A 56-week, double-blind, phase 3a, randomised trial