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Multiple studies in humans and mouse models indicate 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. In the current study, a team discovered that restoring normal sleep by returning to normal the activity of the thalamic reticular nucleus (TRN), a brain region involved in maintaining stable sleep, reduced the accumulation of A-beta plaques in the brain. The study 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...

Using a new mouse model of Alzheimer's disease, researchers at Mount Sinai School of Medicine have found that Alzheimer's pathology originates in Amyloid-Beta (Abeta) oligomers in the brain, rather than the amyloid plaques previously thought by many researchers to cause the disease. The study, which was supported by the "Oligomer Research Consortium" of the Cure Alzheimer Fund and a MERIT Award from the Veterans Administration, appears in the journal Annals of Neurology. "The buildup of amyloid plaques was described over 100 years ago and has received the bulk of the attention in Alzheimer's pathology," said lead author Sam Gandy, MD,...

For years, a prevailing theory has been that one of the chief villains in Alzheimer’s disease has no real function other than as a waste product that the brain never properly disposed of. The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognizing friends and family. But now researchers at Harvard suggest that the protein has a real and unexpected function — it may be part of the brain’s normal defenses against invading bacteria and other microbes....