Deep Sleep May Mitigate Alzheimer’s Memory Loss

Deep sleep can act as a cognitive reserve factor that may increase resilience against beta amyloid proteins in the brain that are linked to memory loss that is caused by dementia. This recent study reveals that superior amounts of deep, slow-wave sleep can act as a protective factor against memory decline among those with existing high levels of AD pathology. 

“With a certain level of brain pathology, you’re not destined for cognitive symptoms or memory issues,” said Zsófia Zavecz, a postdoctoral researcher at UC Berkeley’s Center for Human Sleep Science. “People should be aware that, despite having a certain level of pathology, there are certain lifestyle factors that will help moderate and decrease the effects.

“One of those factors is sleep and, specifically, deep sleep.”

Cognitive reserved factors like years of education, physical activity, and social engagement are believed to help build up resilience to severe brain pathology, keeping the mind sharp despite decreasing brain health. Sleep researchers are also investigating the idea of cognitive reserves as a potential target for protecting memory.

“If we believe that sleep is so critical for memory,” Walker said, “could sleep be one of those missing pieces in the explanatory puzzle that would tell us exactly why two people with the same amounts of vicious, severe amyloid pathology have very different memory?”

“If the findings supported the hypothesis, it would be thrilling, because sleep is something we can change,” he added. “It is a modifiable factor.”

For this study, 62 healthy older participants enrolled in the Berkeley Aging Cohort Study without a dementia diagnosis were recruited. Participants slept in a lab setting while their sleep waves were monitored with an EEG machine. PET scans were used to measure the amount of amyloid deposits in their brains, revealing that half of the participants had deposits and the other half did not.

After sleeping the participants completed memory testing. Those with high amounts of deposits in their brain who had higher levels of deep sleep performed better in testing than their counterparts who had worse sleep. However, this boost was only observed in those with amyloid deposits, as those without pathology experienced no additional supportive effect on memory with deeper sleep. 

These findings remained after controlling for other cognitive reserve factors, suggesting that sleep, independent of the other factors, contributes to protecting memory function in the presence of brain pathology, demonstrating the importance of non-REM slow-wave sleep in counteracting some of the memory-impairing effects of beta-amyloid deposits. 

“Think of deep sleep almost like a life raft that keeps memory afloat, rather than memory getting dragged down by the weight of Alzheimer’s disease pathology,” Walker said. “It now seems that deep NREM sleep may be a new, missing piece in the explanatory puzzle of cognitive reserve. This is especially exciting because we can do something about it. There are ways we can improve sleep, even in older adults.”

“One of the advantages of this result is the application to a huge population right above the age of 65,” Zavecz said. “By sleeping better and doing your best to practice good sleep hygiene, which is easy to research online, you can gain the benefit of this compensatory function against this type of Alzheimer’s pathology.”

Deep sleep could be to the rescue, but more research is required to make definite conclusions. Yet these findings open the door for longer-term research with a larger population to investigate sleep enhancement treatments that could have far-reaching implications to an aging population.