Can poor sleep lead to Alzheimer’s or dementia? – wtkr.com
One in three Americans doesn’t get enough sleep, and 45% of the world’s population doesn’t either.
The US Centers for Disease Control and Prevention calls that a “public health problem,” because disrupted sleep is associated with a higher risk of conditions including diabetes, stroke and cardiovascular disease.
What about Alzheimer’s and other forms of dementia?
It’s well known that people with Alzheimer’s suffer sleep issues. Insomnia, nighttime wandering and daytime sleepiness are common for them, as well as other cognitive disorders such as Lewy body dementia and frontal lobe dementia.
But could poor sleep earlier in life actually cause dementia?
REM sleep and dementia
A new study in the journal Neurology, the journal for the American Academy of Neurology, finds that people who get less REM, or dream-stage sleep, may be at higher risk for developing dementia. REM is the fifth stage of sleep, when the eyes move, the body heats up, breathing and pulse quicken and the mind dreams.
Researchers followed 321 people with an average age of 61 for a dozen years, as part of the famous Framingham Heart Study. Sleep cycles were measured for each person, and their cognitive skills were assessed in person at regular intervals. Over the duration of the study, 32 people developed dementia. Of those, 24 were determined to be Alzheimer’s disease.
The study found that people who took longer than the typical 90 minutes to enter REM were more likely to get dementia. They also spent only about 17% of their sleep dreaming, compared to 20% in those who did not develop dementia.
No association with dementia was found for any of the other four stages of sleep.
“Our findings point to REM sleep as a predictor of dementia,” study author Matthew P. Pase, of Swinburne University of Technology in Australia, said in a news release. “The next step will be to determine why lower REM sleep predicts a greater risk of dementia. By clarifying the role of sleep in the onset of dementia, the hope is to eventually identify possible ways to intervene so that dementia can be delayed or even prevented.”
Sleep and Alzheimer’s plaques
A growing body of research in both mice and humans shows that disturbed sleep leads to higher levels of soluble beta amyloid, the protein that folds and forms the sticky plaques that kill brain cells and bog down information processing.
Depositing amyloid in brain tissue is the first known preclinical stage of Alzheimer’s and happens well before any obvious symptoms of dementia begin.
A few studies in cognitively normal people and one in mice have shown a connection between chronic sleep disruption and the development of amyloid plaques. The research in mice was particularly interesting because it showed that mice who slept well reduced their levels of beta amyloid, effectively clearing the toxin from their brains.
A study in Neurology looked at the relationship between sleep quality and levels of various proteins and inflammatory markers in the cerebrospinal fluid of 101 cognitively healthy adults with an average age of 63.
All participants had known risk factors for Alzheimer’s, such as family history or evidence of the APOE gene, which is associated with a greater chance of developing the disease. Their sleep quality was rated on a standard scale that measured amount, quality and trouble sleeping, along with daytime drowsiness and naps.
“Participants in our study were willing to undergo a lumbar puncture to move research on Alzheimer’s disease forward,” said co-author Barbara Bendlin of the Wisconsin Alzheimer’s Disease Research Center. “Analyzing this fluid allowed us to look at markers related to Alzheimer’s disease such as plaques and tangles, as well as markers of inflammation and nerve cell damage.”
Tangles and cell damage
Tangles are created by damaged tau, a protein responsible for cell stability and structure. Recent research points to tau-tangle accumulation as a possible step beyond amyloid plaques in the development of actual signs of Alzheimer’s disease.
By comparing the spinal fluid against self-reported sleep problems, Bendlin and her colleagues found that the subjects who had sleep issues were more likely to show evidence of tau pathology, brain cell damage and inflammation, even when other factors like depression, body mass, cardiovascular disease and sleep medications were taken into account.
“Our findings align with the idea that worse sleep may contribute to the accumulation of Alzheimer’s-related proteins in the brain,” Bendlin said. “The fact that we can find these effects in people who are cognitively healthy and close to middle age suggest that these relationships appear early, perhaps providing a window of opportunity for intervention.”