The build-up of tau protein is thought to stop brain regions which help to control awakeness from working, the authors of the study published in the journal Alzheimer's and Dementia said. However, amyloid protein, which is also associated with the neurocognitive disorder, didn't appear to play a role.
In the brains of 20 deceased people, 13 with Alzheimer's and seven healthy, the team studied levels of tau protein and counted neurons in three brain regions which help us stay awake.
Researchers found tau had collected in these three regions in those with Alzheimer's, the most common form of dementia, and that 75 percent of neurons had diminished.
The team also looked at seven brains of patients with two other forms of dementia: progressive supranuclear palsy and corticobasal disease. These brains didn't have damage in these regions, suggesting Alzheimer's disease may affect the brain in a unique way.
Jun Oh, lead author of the study and research associate at the Grinberg Lab at the University of California, San Francisco (UCSF), told Newsweek: "[The study] highlights how multifaceted Alzheimer's disease really is. When people, especially outside of the medical field, hear about Alzheimer's disease, they only think about memory problems.
"However, over the past few years, our lab and many others have shown that neuropsychiatric symptoms, especially problems related to sleep and wakefulness, arise in Alzheimer's disease, even before cognitive decline. In this particular paper, we provide compelling evidence that a whole network of neurons that keep us awake are annihilated," he said.
Study co-author Dr. Lea Grinberg, associate professor of neurology and pathology at the UCSF Memory and Aging Center, told Newsweek that people who develop Alzheimer's usually see changes in their sleep patterns years before they show memory changes, tending to sleep more during the day, taking naps, feeling sleepy, or waking up during the night, causing fragmented sleep.
"Besides being very annoying and impacting the person's quality of life, it was unclear if this sleep dysfunction was a risk to develop Alzheimer's or even an early symptom," explained Grinberg.
Past studies suggested that fragmented sleep was caused by mechanical problems leading to sleep apnea. This in turn was thought to cause a build-up of amyloid, affecting brain waves and causing more sleep problems. It was thought daytime sleepiness compensated for the lack of sleep.
"Our study shows that actually, the daytime sleepiness is a primary event caused by degeneration of the wake-promoting neurons rather than a reaction to the fragmented sleep, as such, the treatment should be different." Instead of attempting to clear amyloid plaque, treatments should target tau protein, she argued.
"The study supports the idea that sleep dysfunction is a manifestation of Alzheimer's pathology buildup in the brain, rather than a risk factor. It opens opportunities to treat the cause rather than the symptoms," she said.
However, Grinberg pointed out the study was limited in two ways: the team didn't know how the subjects slept, and could not directly measure neuronal function.
"There is no method available to measure individual neuronal function in humans because it requires introducing electrodes in the brain of living people," she explained.
Asked whether those who nap a lot in the daytime should be worried, Grinberg said: "At this point, it is too premature to get screened for Alzheimer's because of excessive napping because there is no treatment."
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