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.
Alzheimer's and diabetes are two diseases that are increasing at an alarming rate within the U.S. population. Alzheimer's affects one in 10 Americans over 65 years of age and nearly 50 percent of those over 85. Similarly, more than 8 percent of Americans (approximately 26 million people) have diabetes, with the vast majority of those individuals being over 60.
Maher says her team is uncertain of the precise mechanism behind the increase in Abeta and tau in the mouse brain, but their data sugge
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| Contact: Andy Hoang AHoang@salk.edu 619-861-5811 Salk Institute Source:Eurekalert |