Identifying age-related sleep deprivation vulnerability window for prevention of Alzheimer's disease | Matthew Walker
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The decline of deep, slow-wave sleep begins early in life, and by the time a person is in their 80s, their deep sleep brain waves are almost undetectable. The fact that poor sleep is linked with the aggregation of amyloid-beta plaques in the brain and Alzheimer's disease is not surprising. Although some strategies for improving the quality of sleep among people with Alzheimer's have been identified, this might be too late to turn the tide of cognitive decline. But new research is focused on identifying certain windows of vulnerability during a person's life when interventions might improve sleep quality and confer a kind of resilience to Alzheimer's disease, staving off the cognitive decline commonly associated with aging. In this clip, Dr. Matthew Walker talks about the importance of identifying early-life windows of vulnerability to prevent or delay age-related cognitive decline.
Matt: Now I suspect that when the disease is in play and you've been diagnosed in those late stages, I don't know how much sleep is electrically charged even as it may be could help. What we're now trying to do in our studies is actually retrospectively find out, is there a particular decade of life or decades of life when a decline in sleep makes you most susceptible to then developing a lot more amyloid later in life? In other words, we're trying to now identify these vulnerability windows during the lifespan.
The reason I want to do that is, if I can scientifically convince myself of a knowledge base of vulnerability sensitivity to insufficient sleep, my guess is that it's just across the lifespan, it gives me a chance to know where is the inflection point of not late-stage life treatment but early-life prevention. Because that's what medicine has to do right now, I think. We've done a good job at extending lifespan but a miserable job at extending healthspan. Lifespan is probably about treatment. Healthspan is probably about prevention.
Sleep needs to be part of that discussion. And sleep is usually absent in many of these conversations for either lifespan or healthspan despite it having a demonstrable impact on both. But my hope is that to be able to find that sensitive time when your risk for Alzheimer's development by way of insufficient sleep is present. That's where I go in and start augmenting your sleep with electrical brain stimulation or other methods that we're trying to develop as well.
Rhonda: I think, at least for the APOE-4-positive individuals, by the age of 40, the amyloid plaques start to really...
Matt: That's right, yup.
Rhonda: ...you know. So, to me, it would seem that, you know, before 40, and certainly, when you hit 40, you better have your sleep optimized.
Matt: I would say before. I mean, we can see the decline of deep sleep occurring in people in their 20s. That's when your deep sleep starts to decline.
Rhonda: Wow.
Matt: Which is, you know, frightening, isn't it? It's sad. And at that point, it's in the mail. You know, by the time you're 50 years old, you've lost about 50% of the deep sleep that you are having when you are a young teenager. By the time you're 70%, there's only about 5%...sorry, by the time you're 70 years old, there's only about 5% of your deep sleep left that you had when you were young and healthy. By the time you're 80, we almost can't detect any of these deep sleep brain waves anymore.
A neurodegenerative disorder characterized by progressive memory loss, spatial disorientation, cognitive dysfunction, and behavioral changes. The pathological hallmarks of Alzheimer's disease include amyloid-beta plaques, tau tangles, and reduced brain glucose uptake. Most cases of Alzheimer's disease do not run in families and are described as "sporadic." The primary risk factor for sporadic Alzheimer's disease is aging, with prevalence roughly doubling every five years after age 65. Roughly one-third of people aged 85 and older have Alzheimer's. The major genetic risk factor for Alzheimer's is a variant in the apolipoprotein E (APOE) gene called APOE4.
One of three common genetic variants of the APOE (apolipoprotein E) gene. The APOE4 allele, which is present in approximately 10-15% of people, increases the risk of developing Alzheimer's disease and lowers the age of onset. Having one copy of E4 increases risk 2- to 3-fold, while having two copies increases risk as much as 15-fold.
The years of a person’s life spent free of disease.
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