Excessive daytime napping could be early indicator of Alzheimer’s disease, study says
LOS ANGELES - Napping too much during the day could be an early sign of Alzheimer’s disease, a study published this month found.
Areas of the brain that keep a person awake in daytime hours are damaged in the early stages of the disease, HealthDay News reported, citing the study.
For the study, researchers analyzed the brains of 13 deceased Alzheimer’s patients and seven people without the disease. The findings were published Aug. 12 in “Alzheimer’s and Dementia,” the journal of the Alzheimer’s Association.
Alzheimer’s disease attacks brain regions responsible for wakefulness during the day, the researchers found, adding that wakefulness-promoting neurons in these regions are among the first to be damaged by the disease.
Scientists also found that damage to the brain regions involved in daytime wakefulness was caused by a protein called tau, HealthDay News reported. The study provided evidence that the tau protein might play a larger role in the memory-robbing disease than the amyloid protein, which has been more extensively studied, according to the health news outlet.
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Lea Grinberg is an associate professor of neurology and pathology at the Memory and Aging Center and a member of the Global Brain Health Institute at the University of California, San Francisco (UCSF). She is the study’s senior author. "Our work shows definitive evidence that the brain areas promoting wakefulness degenerate due to accumulation of tau — not amyloid protein — from the very earliest stages of the disease," Grinberg said in a UCSF article.
Jun Oh, a Grinberg lab research associate, is the lead author of the study. He and colleagues precisely measured Alzheimer’s pathology, tau protein levels and neuron numbers in the three brain regions involved in promoting wakefulness: the locus coeruleus (LC), lateral hypothalamic area (LHA) and tuberomammillary nucleus (TMN), according to the UCSF article.
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Oh and his colleagues found that the brains of Alzheimer’s patients had “significant tau buildup” in all three of the wakefulness-promoting brain centers compared to the brains of those without the disease. The three regions had lost as much as 75 percent of their neurons, the UCSF article reported.
“It’s remarkable because it’s not just a single brain nucleus that’s degenerating, but the whole wakefulness-promoting network,” Oh said in the article. “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 said that it seems the “wakefulness-promoting network is particularly vulnerable” in Alzheimer’s disease and that “understanding why this is the case is something we need to follow up in future research.”
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“Our new evidence for tau-linked degeneration of the brain’s wakefulness centers provides a compelling neurobiological explanation for those findings,” Grinberg said. “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.”
The study’s authors said increased focus on the role of tau in Alzheimer’s disease suggests that treatments currently in development at UCSF’s Memory and Aging Center and elsewhere directly tackling tau pathology have the potential to improve sleep and other early symptoms of the disease, as well as slow the progress of the disease overall, according to the article.
“This research adds to a growing body of work showing that tau burden is likely a direct driver of cognitive decline,” Grinberg said.