WASHINGTON (Dispatches) -- Restoring normal sleep by returning to normal the activity of the thalamic reticular nucleus (TRN), a brain region involved in maintaining stable sleep, reduces the accumulation of A-beta plaques in the brain, according to a team of researchers.
The study conducted at Baylor College of Medicine in humans and mouse models show that sleep disruptions raise the risk of Alzheimer’s disease (AD) by increasing the accumulation of disease-relevant proteins such as amyloid-beta (A-beta) in the brain. It suggests that TRN not only may play a previously unsuspected driving role in symptoms associated with Alzheimer’s, but also that restoring its normal activity could be a potential therapeutic approach for this severe condition.
Dr. Jeannie Chin, associate professor of neuroscience at Baylor said that they observed in an animal model that TRN activity was generally reduced when compared to the TRN activity of animals without the condition.