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Aging memory loss tracks deep sleep
The disruption of deep sleep is perhaps an underappreciated factor contributing to cognitive or memory decline in aging, and it has recently been found in Alzheimer's disease as well.
Other factors tied to aging and dementia, such as changes in the physical structure of the brain or in its vasculature, are fiendishly difficult to treat, and medicine has no good wholesale approaches to them. Sleep as a missing piece in the explanatory puzzle is exciting because something may be done about it.
Sleeping pills are blunt instruments that do not produce naturalistic sleep, and they have been associated with a higher risk of death and cancer.
How might sleep relate to Alzheimer's disease?
During sleep, the brain's cleanup system moves fluid through spaces between cells and flushes out waste. In a 2013 study in Science, Maiken Nedergaard and colleagues at the University of Rochester found that these spaces expanded by about 60 percent in sleeping mice. The waste includes amyloid-beta, a protein that forms the plaques seen in Alzheimer's disease. In 2018, researchers at the National Institutes of Health found that amyloid in the brain rose in people after a night without sleep.
How is deep sleep identified in a sleep lab?
Technicians place electrodes on the scalp and record electrical activity of the brain in thirty-second segments. Deep sleep appears as large, slow waves of about 0.5 to 4 cycles per second. Under standard scoring rules, it is called stage N3 once these waves fill a set share of each segment. Young adults typically get more of it than older adults.
Why is brain structure so hard to treat in aging?
Neurons in the adult brain are replaced only to a very limited degree, so lost tissue does not simply regrow. Damaged blood vessels in the brain are also hard to repair once the damage is widespread. Most drugs approved for dementia ease symptoms rather than rebuild tissue. This is why researchers look for contributors, such as sleep, that can be changed.
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