Table of Contents
Pharmaceuticals, Volume 11, Issue 1 (March 2018)
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Cover Story (view full-size image) Briefly, amyloid β 1–42 (Aβ) binds to the brain insulin receptor (IR) and dysregulates its [...] Read more. Briefly, amyloid β 1–42 (Aβ) binds to the brain insulin receptor (IR) and dysregulates its signalling cascade in the hippocampus and other brain areas, contributing to the development of insulin resistance. In addition, Aβ indirectly modulates IR activation through the phosphorylation of IR substrates 1 (IRS-1) at its inactivation sites. This response would be the consequence of the increase in reactive glia induced by Aβ and the subsequent release of molecules like tumour necrosis factor alpha (TNFα). Decreased IR signalling leads to reduced activation of protein kinase B (PKB/AKT) which influences other pathways like those controlled by glycogen synthase kinase 3β (GSK3β) and the trafficking of the insulin-sensitive glucose transporter type 4 (GLUT4) to the plasma membrane. In conclusion, all these interrelated mechanisms eventually lead to the well-known memory impairment characteristic of Alzheimer’s disease. View this paper