In a new study, researchers have identified a protein that may contribute to the progression of Alzheimer’s disease pathology in type-2 diabetes.
The finding could have implications for future drug development.
The research was conducted by a team from the University of Illinois at Chicago.
More than 95% of the Alzheimer’s patients have the sporadic late-onset form. But the cause of sporadic, late-onset Alzheimer’s disease is unknown.
Patients with type-2 diabetes have a considerably higher incidence of cognitive decline and AD compared to the general population.
This may provide a clue to its origin.
In the new study, the team examined the relationship between diabetes and Alzheimer’s disease in male mice and human brain tissue.
They found that a protein called caveolin-1 (Cav-1) is depleted in the temporal lobe of humans with diabetes and in a diabetic mouse model.
Depletion of Cav-1 causes the upregulation of amyloid precursor protein and b-amyloid levels.
Importantly, the team showed that restoring Cav-1 levels in mice reduced Alzheimer’s pathology and improved learning and memory deficits.
This finding reveals a potential mechanism responsible for the increased risk of Alzheimer’s disease.
It may help develop a new treatment for brain disease.
The lead author of the study is Jacqueline A. Bonds, Department of Anatomy and Cell Biology.
The study is published in the Journal of Neuroscience.
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