Scientists from Washington University in St. Louis found that lack of sleep could help promote the development of Alzheimer’s disease.
The first study shows that different forms of a key Alzheimer’s protein known as tau arise in a predictable sequence as the disease develops, starting more than 20 years before symptoms appear.
The second study shows that lack of sleep increases levels of a particular form of tau that is harmful.
The research is published in Nature Medicine and Annals of Neurology and was conducted by Randall J. Bateman et al.
Alzheimer’s disease is the most common form of dementia, affecting more than 5 million people in the US, but doctors have limited advice on how to protect against it.
The disease develops silently in the brain for two decades or more before people begin showing the characteristic signs of forgetfulness and confusion.
Understanding that the silent phase could be key to preventing this devastating condition.
The new findings help explain why poor sleep is linked to an increased risk of Alzheimer’s dementia and could lead to ways to identify where people stand on the road to Alzheimer’s.
Alzheimer’s disease is linked to two main proteins: amyloid and tau. Both are normal brain proteins that become harmful when they collect into clumps. Amyloid plaques first appear two decades or more before cognitive symptoms arise.
Tau tangles form later, just as the damage becomes visible on brain scans and cognitive skills begin to decline.
The team suspected that tau might start undergoing changes very early in the disease process that eventually result in the formation of tangles—and cognitive decline.
They studied people enrolled in the Dominantly Inherited Alzheimer Network (DIAN). Such participants have rare genetic mutations that cause them to develop Alzheimer’s at young ages, around the same ages their parents developed the disease.
While devastating for families, these mutations allow researchers to know who will develop the disease and when.
The researchers analyzed samples of cerebrospinal fluid—the fluid that surrounds the brain and spinal cord—from 370 participants.
The researchers found that phosphorylated tau-217—arose 21 years before the expected age of symptom onset and stayed high until just before signs of cognitive decline became detectable.
They also examined the effect of sleep on phosphorylated tau. Poor sleep, such as sleep apnea, has been linked to the risk of developing Alzheimer’s dementia.
The researchers studied eight people ages 30 to 60 with no sleep or cognitive problems.
The participants were assigned randomly to one of three conditions: having a normal night’s sleep without any sleep aids; staying up all night; or sleeping after treatment with sodium oxybate, a prescription medication for sleep disorders.
The researchers took samples of the fluid that surrounds the brain and spinal cord every two hours over a 36-hour period to monitor how tau phosphorylation patterns change with time of day and different sleep conditions.
The team found after a sleepless night, phosphorylated tau-217 in the cerebrospinal fluid rose 60% to 80% over baseline levels.
There was no such rise after a night of normal sleep or after sleeping with the aid of a drug.
The team says the changes to tau phosphorylation in this study could explain how sleep deprivation promotes the development of Alzheimer’s disease.
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