- Researchers have discovered that when a protein form tangles, it can kill nerve cells, destroying parts of the brain responsible for maintaining wakefulness.
- The researchers theorize this is why excessive daytime sleepiness may be a symptom of Alzheimer’s disease.
- Experts say that poor sleep patterns can also cause these protein tangles to form, and getting sufficient sleep is an important way to reduce the risk of developing Alzheimer’s disease.
While an occasional nap can help us get through the day, excessive daytime sleepiness could be a sign of increased risk for Alzheimer’s disease.
In the study, scientists measured signs of Alzheimer’s disease in the brain regions associated with promoting wakefulness in 13 deceased individuals with Alzheimer’s disease and compared them to 7 people who didn’t have it.
The researchers obtained the data from the UCSF Neurodegenerative Disease Brain Bank.
Tau is a protein normally found within nerve cells that helps form structures that move nutrients within nerve cells.
When this happens, the microtubules can no longer transport nutrients and other essential substances in nerve cells, leading to cell death.
“In this particular study, we were curious if a specific network within the brain stem and subcortical regions are affected in Alzheimer’s disease. We found that the network, which [promotes] wakefulness, is obliterated in Alzheimer’s disease,” Joseph Oh, the study’s lead author and a staff research associate in the Grinberg Lab Memory and Aging Center at the Weill Institute for Neurosciences at UCSF, told Healthline.
“These regions have been historically less focused on in Alzheimer’s disease research. However, we and several others have shown that these regions are highly involved in the disease pathogenesis,” he said.
The new findings are in line with those of an earlier study by the Grinberg lab showing that people who died with elevated tau protein levels in their brain stem had already begun experiencing increased sleep disturbances as well as changes in mood such as anxiety and depression.
“I think the extent of substantial neuronal loss in the wake-promoting centers was very surprising and, in a way, frightening,” Oh said. “This is especially true because not just one type of neuron is affected, but an entire wake-promoting network.”
Rong Zhang, PhD, director of the cerebrovascular laboratory at the Institute for Exercise and Environmental Medicine at Texas Health Presbyterian Hospital and UT Southwestern Medical Center in Dallas, did issue some cautionary words about the research.
On the other hand, Dr. Steven Lin, DO, a board-certified neurologist specializing in neurology and sleep medicine at Healthcare Associates in Medicine in New York, said sleep and Alzheimer’s disease seem to be tied together.
Another recent study by psychologists at the University of California Berkeley, concluded that people in their 50s and 60s who report a declining quality of sleep also have more protein tangles in their brain.
“Insufficient sleep across the lifespan is significantly predictive of your development of Alzheimer’s disease pathology in the brain,” Matthew Walker, PhD, the study’s senior author and a sleep researcher and professor of psychology at Harvard Medical School in Massachusetts, said in a statement.
“Unfortunately there’s no decade of life that we were able to measure during which you can get away with less sleep,” Dr. Walker said. “There’s no ‘Goldilocks decade’ during which you can say, ‘This is when I get my chance to short my sleep.’”
Whether poor sleep causes tau protein tangles or the tangles cause poor sleep still isn’t fully understood, but Lin said there are simple guidelines that can be followed to generally improve how well we sleep:
- Make your bedroom an environment that’s conducive to sleep.
- Go to bed and wake up at around the same time every day.
- Engage in physical activity during the day, which can increase nighttime sleepiness.
- Get adequate light exposure during the day.
- Follow a healthy diet.
Drugs such as diphenhydramine are anticholinergic and block an important neurotransmitter called acetylcholine.