Posted on Jul 16, 2020, 2 p.m.
A recent study published in Alzheimer’s & Dementia suggests that Alzheimer’s disease may kill off cells that are needed to stay awake, which may explain why those living with this debilitating and brain wasting disease nap so much.
The study found that tau proteins promote the degeneration of brain regions that are responsible for keeping people awake, this may help to explain why excessive daytime napping is so common among those with this disease, and it may also suggest that this might be an early sign of the disease.
This link has been explored in previous research with some considering napping to be the brain’s way of compensation for poor nighttime sleeping that can be caused by related disruptions, and others suggesting that the sleep problems themselves are what causes the disease to progress.
In collaboration, researchers from the University of California and the University of Sao Paolo Brazil in this study showed that there is a direct connection between excessive daytime napping and Alzheimer’s disease; as well as showing that tau protein tangles play a larger role in the disease than the more frequently associated amyloid plaques.
The brains of 13 deceased Alzheimer’s disease patients were examined and compared to the brains of 6 healthy brains, measuring for Alzheimer’s pathology, tau protein levels, and the number of neurons present in 3 brain regions that are associated with wakefulness; the lateral hypothalamic area, the tuberomammillary area, and the locus coeruleus: All three of these brain regions were found to have significant tau buildup which caused those regions to lose as much as 75% 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.
Additionally, the team also studied brain samples from 7 individuals with different forms of tau related dementia, and unlike what was seen in the Alzheimer’s patients the tau buildup did not affect the neural networks that are associated with wakefulness within these individuals.
Findings suggest that wakefulness promoting neurons may be particularly vulnerable to the harmful effects of the tau aggregation only in Alzheimer’s disease, leading the team to suggest that excessive daytime napping may be an early symptom of the disease especially if it is not accompanied by or caused by significant sleep problems at night.
In other research Lea Grinberg, who is this study’s co-author, investigated whether amyloid plaques or tau tangles are linked to neuropsychiatric symptoms like agitation, anxiety, appetite changes, depression, and sleep disturbances that often precede the more common signs of Alzheimer’s disease. In that study the team found no association between amyloid plaques and mood related symptoms, but they did find tau tangles were already present in the brainstems of those with early stage disease that were lacking in memory changes but had increased rates of one or more neuropsychiatric symptoms.
According to Grinberg these findings show that tau proteins and not beta amyloid are involved in the onset of Alzheimer’s disease, and she believes that this work can help researchers to find a way to reduce the burden of this disease 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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