Diabetes Raises Levels of Proteins Linked to Alzheimer’s Features

Growing evidence suggests that there may be a link between diabetes and Alzheimer’s disease, but the physiological mechanisms by which diabetes impacts brain function and cognition are not fully understood. In a new study published in Aging Cell, researchers at the Salk Institute for Biological Studies show, for the first time, that diabetes enhances the development of aging features that may underlie early pathological events in Alzheimer’s.

Specifically, the Salk team found increases in two hallmarks of Alzheimer’s-accumulations of amyloid beta (Abeta) and tau protein-in the brains of diabetic mice, especially in cells surrounding blood vessels. Abeta, the misfolded peptide that is thought in part to cause Alzheimer’s disease, aggregated inside astrocytes, star-shaped brain cells that, upon interaction with Abeta, release inflammatory molecules that can destroy neurons. Previously, this had not been shown in mouse models of type 1 diabetes (T1D).

"Our study supports and extends the links between diabetes, aging and Alzheimer’s," says senior author Pamela Maher, a senior staff scientist in Salk’s Laboratory of Cellular Neurobiology. "We show that type 1 diabetes increases vascular-associated amyloid beta buildup in the brain and causes accelerated brain aging."

The findings suggest that the neurovascular system may be a good candidate for new therapeutic targets to treat Alzheimer’s in the early stages of the disease.