Why do we sleep? And does it matter for AD?

I recall that in the 1970s science was drawing a complete blank on why we sleep. The traditional explanation was that it was an opportunity for the body to repair itself, but no one could find any repairs in progress. The best explanation seemed to be that diurnal animals should be rolled up somewhere safe at night, and nocturnal animals should be doing the same during the day. An imperative for sleep would force this behavior. So it all seemed to hinge on the geometry of the eye. Eyes were designed for either diurnal or nocturnal animals, and there was no design to accommodate both.

But researchers are now going back to the repair concept, and it seems to have implications for our understanding of AD.  In Beating the Dementia Monster, I cited research correlating interrupted and inadequate sleep with increases in beta amyloids in cerebral-spinal fluids.  This strongly suggests a connection between sleep problems and AD.

A recent understanding is that deep sleep (as opposed to “raid eye movement” (REM) sleep) facilitates the removal of waste products from between brain cells. (REM sleep is lighter sleep, and it’s when you dream.) As cells function, they create wastes that are expelled from the cells through their membranes and into the space between them. During deep sleep, the space between the cells expands and allows a fluid system to flush the wastes out of the brain. Here is one study analyzing this. There is a hypothesis that when the wastes build up between the cells and are not flushed out, the presence of the wastes promotes AD.

Another thing to understand about sleep relates to what’s called “plasticity.” Neurons are constantly disconnecting and reconnecting to other neurons as a part of the memory retention process. This process occurs primarily during sleep (including REM sleep), and is important to memory. In AD, sleep patterns are disrupted, complicating the brain’s challenges with respect to memory consolidation and retention.