Previous studies have explored the link between daytime napping and Alzheimer's disease. While some consider it the brain's way of compensating for poor nighttime sleep, which can be caused by Alzheimer's-related disruptions, others argue that the sleep problems themselves are what causes the disease to progress.
In their study, researchers at University of California, San Francisco and the University of Sao Paolo in Brazil showed that there is a direct connection between excessive daytime napping and Alzheimer's disease. They also showed that tau protein tangles play a larger role in Alzheimer's than the more frequently associated amyloid plaques.
Tau proteins are found in neurons and perform important functions, such as stabilizing the microtubules that help transport nutrients and other substances from one part of the nerve cell to another. However, tau dysfunction can cause these proteins to disarrange and misfold in a specific way, forming neurofibrillary tangles that contribute to the development of Alzheimer's disease.
For their study, the researchers examined the brains of 13 deceased Alzheimer's patients and compared them to the brains of seven healthy individuals. They measured Alzheimer's pathology, tau protein levels and the number of neurons present in three brain regions associated with wakefulness, namely, the locus coeruleus, the lateral hypothalamic area and the tuberomammillary nucleus.
The researchers found that in the Alzheimer's patients, all three brain regions had significant tau buildup. This caused those regions to lose as much as 75 percent of the neurons.
"It’s remarkable because it’s not just a single brain nucleus that’s degenerating, but the whole wakefulness-promoting network," said Jun Oh, the lead author of the study.
Oh and his colleagues also studied brain samples from seven individuals with different forms of tau-related dementia. Unlike in the Alzheimer's patients, tau buildup did not affect the neural networks associated with wakefulness in these individuals. (Related: Understanding the medical differences between Alzheimer’s and dementia.)
These findings demonstrate that wakefulness-promoting neurons are particularly vulnerable to the harmful effects of tau aggregation only in Alzheimer's disease. They also suggest that excessive daytime napping may be an early symptom of Alzheimer's, especially if it's not accompanied or caused by significant sleep problems at night.
Previously, scientists have focused most of their attention on amyloid proteins, which are known to form plaques in the brains of Alzheimer's patients. But in an earlier study, Lea Grinberg, Oh's co-author, and her colleagues investigated whether amyloid plaques or tau tangles are linked to neuropsychiatric symptoms, such as agitation, anxiety, appetite changes, depression and sleep disturbances. These symptoms often precede the more common signs of Alzheimer's, including memory problems.
Grinberg and her team found no association between amyloid plaques and mood-related symptoms. However, they found that tau tangles were already present in the brainstems of individuals with early-stage Alzheimer's. Although they lacked memory changes, these individuals had increased rates of one or more neuropsychiatric symptoms.
These findings, according to Grinberg, clearly show that tau proteins, and not beta-amyloid, are involved in the onset of Alzheimer's disease. She also believes that this new knowledge can help researchers find a way to reduce the burden of Alzheimer's in aging adults.
"These results could have major implications for Alzheimer’s drug trials focused on early degenerative changes, where people have been seeking tractable clinical outcomes to target in addition to early cognitive decline," said Alex Ehrenberg, the lead author of the study.
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