By examining the role of cholesterol in Alzheimer’s disease and type 2 diabetes, researchers identified a small molecule that could help regulate cholesterol levels in the brain, making it a potential new therapeutic target for the disease. Alzheimer’s disease.
There is no known cure for Alzheimer’s disease and over the past decade scientists have found a growing body of evidence linking the underlying causes of type 2 diabetes and Alzheimer’s disease. Alzheimer’s.
Type 2 diabetes occurs when insulin becomes less effective at removing glucose from the bloodstream, resulting in high blood sugar which can lead to abnormal cholesterol levels.
A similar situation occurs in Alzheimer’s disease, but rather than affecting the body as a whole, the effects are localized in the brain.
“Alzheimer’s disease and diabetes have many common causes,” said study co-author Gregory Thatcher, a professor in the College of Pharmacy at the University of Arizona.
“Our goal was to develop a way to identify compounds that would counteract many of the damaging changes that contribute to both Alzheimer’s and type 2 diabetes,” Thatcher added.
When cholesterol rises, due to insulin resistance or other factors, the body begins a process known as reverse cholesterol transport, in which specific molecules transport excess cholesterol to the liver. to be excreted.
Apolipoprotein E (APOE) is one of the proteins involved in the reverse transport of cholesterol.
APOE is also the most potent risk factor gene for Alzheimer’s disease and associated dementia, and an independent risk factor for type 2 diabetes and cardiovascular disease.
Likewise, reduced activity of another cholesterol transporter, the ATP binding cassette transporter A1 (ABCA1), correlates with an increased risk of cardiovascular disease, type 2 diabetes, and A. Alzheimer’s.
The increased activity of ABCA1 is expected to positively influence insulin signaling and reduce inflammation in the brain, making it a potential therapy for type 2 diabetes and Alzheimer’s disease.
In this study published in the journal ACS Pharmacology and Translational Science, Thatcher and the research team devised a way to identify small molecules that improve the function of ABCA1 in the body while avoiding adverse effects on the liver.