Hundreds of millions of dollars are spent on dementia research annually. While many may not like my opinion, I think we’re throwing this money away.
To date, we have had very little in the way of a “cure.” The research dollars continue to hit dead ends.
Here’s the problem. By the time that someone is diagnosed with a neurodegenerative disorder, it is likely that he or she has already lost a large chunk of the dopaminergic cells of the substantia nigra (Parkinson’s) or the cells of the hippocampal region and the neocortex (Alzheimer’s dementia). In these patients, the loss of brain cells has been going on for decades. DECADES.
The process is a freight train going.
I do not think we will ever be able to stop this freight train. Slow it down maybe: studies on coenzyme Q10, magnesium, exercise and ginko biloba have demonstrated the ability to slow the progression of neurodegenerative disorders.
One thing, however, is very, very clear.
Prevention is possible. We now have very clear cut risk factors for Alzheimer’s dementia. And the vast majority of them are modifyable. Very modifyable. Smoker? Quit. Don’t exercise? Start. On your way to diabetes? Change your diet and exercise. Too much brainless TV? Shut it off and challenge your mind.
This particular study adds yet another preventable risk factor to the list.
Sleep. And lack of it.
And not just the take-a-pill-so-you-can-sleep sleep, but good quality, slow-wave sleep (SWS, non-REM stage N3). Ironically, some drugs that you may take to help you sleep are actually interfering with your ability to hit the SWS stage of sleep. Drugs like fluoxetine (Prosac) and paroxetine (Paxil) have been shown to interfere with SWS sleep.
Researchers looked at a group of 167 Japanese American men in Honolulu, HI who were followed until their death and had their brains examined at autopsy. Specifically, researchers were looking for signs of brain damage associated with cognitive loss and Alzheimer’s (Braak stage, neurofibrillary tangle and neuritic plaque counts, microinfarcts, generalized brain atrophy, lacunar infarcts, Lewy bodies, neuronal loss and gliosis in the locus ceruleus).
This brain damage was then compared to the results of a sleep study (polysomnography) done at the beginning of the study. Here’s what they found: and died through 2010 (mean 6.4 years to death). Polysomnography measures included the apnea-hypopnea index, duration of apnea or hypopnea, duration of hypoxemia, minimum oxygen saturation (SpO2), duration of slow-wave sleep (SWS, non-REM stage N3), and arousals.
- Sleep duration with oxygen saturation levels (SpO2) less than 95% was associated with a whopping 388% higher levels of microinfarcts (small strokes).
- Greater SWS duration (in other words, better deep sleep) was associated with less 68% less atrophy in the brain.
- Lewy bodies were 83% less common in those who had more sleep at 95% oxygen saturation or more.
- Higher minimum oxygen saturation during REM sleep was associated with less gliosis and neuronal loss in the locus ceruleus (in English–less inflammatory cells and less dead brain cells were found in the region of the brain stem that deals with stress and our ability to respond to stress).
- Cognitive scores declined less among men with greater SWS duration.
These are some pretty serious associations. And it all fits into the picture of what we already know. Prediabetes and diabetes are very closely associated with cognitive loss, dementia and Alzheimer’s. Prediabetes and diabetes are also closely associated with sleep apnea. So it just makes sense that sleep apnea and poor quality sleep would be linked to brain damage.
That sounds serious. AND, it sounds like it’s finally time to go get that sleep study done and find out if you need to be using a CPAP or BiPAP machine. Your brain will thank you.