New research published in BMC Medicine suggests that deep sleep, also known as non-REM slow-wave sleep, could help protect against memory loss in older adults with a high burden of Alzheimer’s disease. The study found that deep sleep acts as a “cognitive reserve factor” that increases resilience against the beta-amyloid protein, which is associated with memory loss in dementia.
The study was motivated by the question of why some people with high levels of Alzheimer’s disease pathology experience significant memory problems, while others with the same level of pathology do not. One possible explanation is the concept of cognitive reserve, which refers to factors that protect against or compensate for the effects of AD pathology on memory.
The researchers focused on a specific factor that could contribute to cognitive reserve: deep non-rapid eye movement (NREM) slow-wave sleep. Previous research has shown that deep sleep is important for learning and memory in healthy older adults. The researchers wanted to investigate whether the quality of deep sleep, specifically the slow-wave activity during deep sleep, could act as a cognitive reserve factor in older adults with Alzheimer’s disease pathology.
“Alzheimer’s disease is one of the most prevalent dementias and thus affects the quality of life of a lot of people (both individuals living with the disease and caregivers),” said study author Zsófia Zavecz, a postdoctoral researcher at UC Berkeley’s Center for Human Sleep Science.
“A significant body of research targets intervention studies to decrease the brain pathology underlying Alzheimer’s disease, but there is an exciting new research direction, where researchers are studying resilience to already existing brain pathology. That is, what factors explain the individual differences in cognitive function despite the same level of brain pathology, and how do some people with significant pathology have largely preserved memory? If we identify modifiable resilience factors, we could relieve some of the cognitive and memory symptoms that affect individuals with Alzheimer’s disease pathology.”
“The specific proposal of sleep as a resilience (or more specifically cognitive reserve) factor stems from previous studies demonstrating the support of sleep for both cognitive and memory performance, as well as its association with Alzheimer’s disease and the underlying brain pathologies,” Zavecz explained. “Sleep is also a modifiable factor, thus if proven to be a resilience factor, we have another intervention target to improve memory performance in individuals with Alzheimer’s disease pathology.”
To conduct the study, the researchers recruited 62 cognitively normal older adults, of which 31 had high levels of beta-amyloid (a hallmark of Alzheimer’s disease) and 31 had low levels. The participants underwent positron emission tomography (PET) scanning to measure their beta-amyloid burden in the brain. They also spent two nights in a sleep lab, where their sleep was monitored using polysomnography (PSG) to measure slow-wave activity during deep sleep.
The researchers also collected data on gray matter atrophy (a measure of brain health) using structural magnetic resonance imaging (MRI). Finally, the participants completed a face-name memory task to assess their memory performance.
The study found that individuals with high levels of beta-amyloid deposits in their brains who also had better quality deep sleep performed better on a memory test compared to those with the same amount of deposits but poor sleep. This suggests that deep sleep, specifically NREM slow-wave activity, can help preserve memory function in individuals with Alzheimer’s pathology. However, this compensatory effect was not observed in individuals without the pathology, as their cognitive function was already intact.
Deep sleep essentially acted as a protective factor, counteracting the negative effects of beta-amyloid on memory. The researchers believe that deep sleep may be an important factor in cognitive reserve. This discovery is promising, the researchers said, because it suggests that improving sleep quality, even in older adults, could potentially help mitigate the impact of Alzheimer’s disease on memory.
“The main take home message is that a good night’s sleep can improve memory function in individuals with early Alzheimer’s disease pathology,” Zavecz told PsyPost. “It is also important that sleep is a modifiable factor, and with simple sleep hygiene steps anyone could improve their sleep at home.”
The researchers also considered different explanations for how deep sleep might support memory function. One possibility is that deep sleep helps restore and normalize synaptic strength in the brain, counteracting the abnormal synaptic potentiation associated with Alzheimer’s pathology.
Another explanation is that deep sleep plays a role in the transformation of memory from the hippocampus to other brain regions, promoting memory consolidation and independence from the hippocampus. Additionally, deep sleep may enhance glymphatic clearance, a process that clears metabolic waste from the brain and is important for cognitive functioning.
But it’s important to note that the study had limitations, including the lack of establishing causality between sleep and memory and the possibility of other factors, such as tau pathology or brain changes, influencing sleep-dependent cognitive reserve. The findings also apply to a relatively healthy cohort and may not be generalized to the entire elderly population or those with Alzheimer’s disease.
“In our study, the participants were healthy older adults with beta-amyloid pathology, which is the first pathological event in the cascade of Alzheimer’s disease,” Zavecz told PsyPost. “The extent to which sleep could offer a protective buffer against severe brain pathology or severe cognitive impairment remains to be tested. However, this study is the first step in hopefully a series of new research that will investigate sleep as a cognitive reserve factor.”
“Further, our study has shown that sleep modifies the effect of beta-amyloid on memory function, however, it did not prove causation. Nevertheless, sleep is a modifiable factor, and intervention studies on boosting sleep are also exciting next steps following this paper.”
The study, “NREM sleep as a novel protective cognitive reserve factor in the face of Alzheimer’s disease pathology“, was authored by Zsófia Zavecz, Vyoma D. Shah, Olivia G. Murillo, Raphael Vallat, Bryce A. Mander, Joseph R. Winer, William J. Jagust, and Matthew P. Walker.
