Amylin is a protein that is co-secreted from pancreatic beta cells alongside insulin and has been shown to cross the blood-brain barrier and impact the formation of amyloid plaques. The normal function of amylin in the brain is directly correlated to metabolism because amylin is considered a satiety protein. The output involved in the metabolic process involves oxidative phosphorylation and includes a set of proteins known as uncoupling proteins (UCPs), which are proteins that directly impact oxidative phosphorylation. Traditionally, UCPs are known to impact the ATP levels that occur in oxidative phosphorylation. However, recently it has been postulated that UCPs may have an additional role that involves cell signaling. In fact, UCP2 has been shown to be present in pancreatic beta cells and to have diminished protein levels in Alzheimer’s disease brains. The experiments conducted in this study analyzed the relationship between UCP2 and amylin. Specifically, immunohistochemistry experiments that examine both the presence of amylin and UCP2 in Alzheimer’s disease brains were conducted. Western Blot analysis experiments were also conducted to compare the findings from the immunohistochemistry experiments.
