Neuroinflammation and neurologic deficits in diabetes linked to brain
accumulation of amylin.
Authors Srodulski S, Sharma S, Bachstetter AB, Brelsfoard JM, Pascual C, Xie XS, Saatman
KE, Van Eldik LJ, Despa F
Submitted By Florin Despa on 8/28/2014
Status Published
Journal Molecular neurodegeneration
Year 2014
Date Published
Volume : Pages 9 : 30
PubMed Reference 25149184
Abstract We recently found that brain tissue from patients with type-2 diabetes (T2D) and
cognitive impairment contains deposits of amylin, an amyloidogenic hormone
synthesized and co-secreted with insulin by pancreatic ß-cells. Amylin
deposition is promoted by chronic hypersecretion of amylin (hyperamylinemia),
which is common in humans with obesity or pre-diabetic insulin resistance. Human
amylin oligomerizes quickly when oversecreted, which is toxic, induces
inflammation in pancreatic islets and contributes to the development of T2D.
Here, we tested the hypothesis that accumulation of oligomerized amylin affects
brain function.


Investigators with authorship
NameInstitution
Florin DespaUniversity of Kentucky

Complications