Figure 6
From: Neuroinflammation and neurologic deficits in diabetes linked to brain accumulation of amylin
Proposed pathological mechanism for the impact of hyperamylinemia on brain function. Pre-diabetic insulin resistance triggers hyperamylinemia (which coincides with hyperinsulinemia) and leads to an increased secretion of oligomerized amylin from pancreatic islets in the blood. Circulating oligomerized amylin infiltrates the blood vessel wall causing blood–brain barrier injury and diffusion of oligomerized amylin in the brain, where it is toxic to the neuron. These pathological processes begin in pre-diabetes and may ignite the development of neurological deficits.