UC Davis researchers have found deposits of a protein that accumulates in the brains of patients with type 2 diabetes inside the brains of people with Alzheimer’s disease.
The protein, called amylin, is secreted with insulin and travels through the bloodstream to the brain. It also accumulates in the brains of individuals with dementia.
Because it does so in the same manner as plaques called amyloid beta associated with Alzheimer’s disease, amylin could serve as a new biomarker for age-releated dementia and Alzheimer’s, according to the study, published online in the Annals of Neurology.
“We’ve known for a long time that diabetes hurts the brain, and there has been a lot of speculation about why that occurs, but there has been no conclusive evidence until now,” said UCD Alzheimer’s Disease Center Director Charles DeCarli, in a news release.
“This research is the first to provide clear evidence that amylin gets into the brain itself and that it forms plaques that are just like the amyloid beta that has been thought to be the cause of Alzheimer’s disease. In fact, the amylin looks like the amyloid beta protein, and they both interact.”
The research was conducted using tissue from the brains of individuals over 65 donated to center.
The researchers found amylin deposits in the gray matter and walls of the blood vessels in the brains of diabetic patients with dementia. They also found amylin in the brain tissue of Alzheimer’s patients who had not been diagnosed with diabetes, suggesting those individuals may have had undiagnosed insulin resistance.
They did not find amylin deposits in the brains of health control subjects.
Florin Despa, assistant professor-in-residence in the department of pharmacology, said the finding may offer a therapeutic target for drug development.
“If we’re smart about the treatment of pre-diabetes, a condition that promotes increased amylin secretion, we might be able to reduce the risk of complications, including Alzheimer’s and dementia,” he said.