Extreme drowsiness during the day is a common sign of Alzheimer’s disease, but what causes it? We now have an answer thanks to a recent study.
Even after a full night’s sleep, many persons with Alzheimer’s disease have a tendency to sleep a lot during the day.
Researchers believe that looking at daytime napping patterns could help predict the onset of Alzheimer’s disease, based on correlations between excessive drowsiness and neurodegenerative disorders.
But it’s still unclear why persons with this illness feel the urge to sleep so frequently.
A recent study led by experts at the University of California, San Francisco (UCSF) and other institutions reveals that individuals with Alzheimer’s disease suffer significant brain cell loss in regions of the brain responsible for keeping us awake.
The findings, which were published in the journal Alzheimer’s & Dementia, also point to an overabundance of tau protein as a possible cause of these abnormalities in the brain.
In Alzheimer’s disease, tau proteins form tangles that make it hard for neurons (brain cells) to communicate with each other and hurt cells.
Senior author Dr. Lea Grinberg says that this study “shows definitive evidence that the brain areas promoting wakefulness degenerate due to accumulation of tau — not amyloid protein [another protein that can become toxic in Alzheimer’s disease] — from the very earliest stages of the disease.”
Dr. Grinberg and his colleagues examined the brains of 13 persons who died of Alzheimer’s disease, as well as seven people who died of other causes. The samples were taken from the UCSF Neurodegenerative Disease Brain Bank.
The researchers discovered that, when compared to healthy brains, Alzheimer’s patients had high levels of tau in three crucial locations for staying awake: the locus coeruleus, the lateral hypothalamic area, and the tuberomammillary nucleus. Not only that, but these regions had actually lost 75% of their neurons as a result of the disease.
“It’s remarkable because it’s not just a single brain nucleus that’s degenerating, but the whole wakefulness-promoting network,” adds the study’s lead author, Jun Oh.
“Crucially, 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,” Oh says.
The researchers next performed a postmortem examination of brain tissues from seven persons with progressive supranuclear palsy and corticobasal disease in order to gain more insight. These are two types of dementia that are distinguished by the overabundance of tau protein.
The investigators found no evidence of the same loss of neurons in areas associated with states of wakefulness in these samples, suggesting that this damaging loss is limited to Alzheimer’s disease.
“It seems that the wakefulness-promoting network is particularly vulnerable in Alzheimer’s disease. Understanding why this is the case is something we need to follow up in future research,” adds Oh.
Dr. Grinberg and colleagues previously discovered evidence that tau protein may have a direct impact on Alzheimer’s disease brain deterioration. The researchers discovered that persons who died with high levels of tau in their brain stem — a sign of early-stage Alzheimer’s disease — had started to experience mood swings and sleep issues.
“Our new evidence for tau-linked degeneration of the brain’s wakefulness centers provides a compelling neurobiological explanation for those findings,” adds Dr. Grinberg.
“It suggests 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.”
“This research adds to a growing body of work showing that tau burden is likely a direct driver of cognitive decline,” says Dr. Lea Grinberg.
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