I reported a few months ago on some evidence of a link between disturbed sleep and the development of Alzheimer’s. Now a mouse study adds to this evidence.
The mouse study follows on from an earlier study showing that brain levels of amyloid beta naturally rise when healthy young mice are awake and drop after they go to sleep, and that sleep deprivation disrupted this cycle and accelerated the development of amyloid plaques. This natural rhythm was confirmed in humans.
In the new study, it was found that this circadian rhythm showed the first signs of disruption as soon as Alzheimer’s plaques began forming in the mice’s brains. When the genetically engineered mice were given a vaccine against amyloid beta, the mice didn’t develop plaques in old age, the natural fluctuations in amyloid beta levels continued, and sleep patterns remained normal.
Research with humans in now underway to see whether patients with early markers of Alzheimer’s show sleep problems, and what the nature of these problems is.
Just to make it clear: the point is not so much that Alzheimer’s patients are more likely to have sleep problems, but that the sleep problems may in fact be part of the cause of Alzheimer’s disease development. The big question, of course, is whether you can prevent its development by attacking the dysfunction in circadian rhythm. (See more on this debate at Biomed)
(2012). Disruption of the Sleep-Wake Cycle and Diurnal Fluctuation of β-Amyloid in Mice with Alzheimer’s Disease Pathology.
Science Translational Medicine. 4(150), 150ra122 - 150ra122.