Previous studies suggest that such sleepiness in Alzheimer’s patients results from poor nighttime sleep due to disease, while others suggest that sleep problems may cause the disease to progress; this study suggests a more direct biological pathway between daytime sleepiness and Alzheimer’s disease.
Researchers studied the brains of 13 individuals with Alzheimer’s disease that had died, and the brains from 7 individuals that did not have the disease. 3 parts of the brain were specifically examined that are involved in keeping us awake: the lateral hypothalamic area; the tuberomammillary area; and the locus coeruleus which all work together in a network to keep us awake during the day.
The number of neurons in these regions were compared between the diseased and healthy brains, as well as levels of tau proteins which build up in the brain and are thought to slowly destroy brain cells and connections between them. Diseased brains were found to have had significant levels of tau tangles in the 3 regions, and the regions has lost up to 75% of their neurons.
“It’s remarkable because it’s not just a single brain nucleus that’s degenerating, but the whole wakefulness-promoting network,” lead author Jun Oh. “This means that the brain has no way to compensate, because all of these functionally related cell types are being destroyed at the same time.”
The Alzheimer’s brain samples were then compared with tissue samples from 7 individuals with other forms of dementia caused by accumulation of tau; results showed that even with the buildup of tau brains with other forms of dementia didn’t show damage to the neurons that promote wakefulness.
“It seems that the wakefulness-promoting network is particularly vulnerable in Alzheimer’s disease,” Oh said in a statement. “Understanding why this is the case is something we need to follow up in future research.”
“…we need to be much more focused on understanding the early stages of tau accumulation in these brain areas in our ongoing search for Alzheimer’s treatments,” senior author Dr. Lea Grinberg.
