Deep Sleep Could Help Mitigate Memory Loss in Alzheimer’s Patients

NREM sleep emerges as a key cognitive reserve factor in the face of Alzheimer's disease pathology

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New research from the University of California, Berkeley, suggests that deep sleep may help buffer against memory loss in older adults with Alzheimer’s disease. Non-REM slow-wave sleep can act as a “cognitive reserve factor” and increase resilience against the beta-amyloid protein linked to dementia.

A new study found that deep sleep acts as a protective factor against memory decline in those with high levels of Alzheimer’s disease pathology. This could potentially lead to new therapies to alleviate the devastating outcomes of dementia.

The study involved 32 healthy adults and 20 adults with early signs of Alzheimer’s disease. Participants were fitted with electrodes to monitor their brain waves while they slept. The researchers found that the participants with Alzheimer’s disease had less slow-wave activity during NREM sleep, which indicated that their brains could not clear away the toxic proteins as efficiently as the healthy adults.

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

The researchers also found that the participants with Alzheimer’s disease who had more slow-wave activity during NREM sleep performed better on memory tests the next day. This suggests that deep sleep may play a crucial role in mitigating the memory loss associated with Alzheimer’s disease.

The findings of this study are particularly significant as they could help pave the way for new treatments for Alzheimer’s disease. While there is currently no cure for the disease, this research highlights the importance of deep sleep for maintaining cognitive function in Alzheimer’s patients. 

The researchers hope that further studies will be conducted to explore the potential of using deep sleep as a therapeutic intervention for the disease.

A new study published in BMC Medicine explores the relationship between cognitive reserve and sleep in the context of Alzheimer’s disease. Alzheimer’s destroys memory and affects daily tasks, with one in nine people over 65 developing the disease.

The study focuses on beta-amyloid deposits and how deep sleep affects their buildup, leading to dementia. Cognitive reserve factors, such as education and social engagement, help keep the mind sharp, but they are not easily changed. The study suggests that deep sleep acts as a cognitive reserve factor, potentially leading to new therapies to combat Alzheimer’s.

Walker said, “If we believe that sleep is so critical for memory,” 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?”

In people with similar amounts of beta-amyloid protein deposits, more deep sleep corresponded with improved memory function. (Illustration courtesy Matthew Walker)

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

Researchers from UC Berkeley studied 62 older adults to investigate the relationship between deep sleep and memory function. The participants were monitored using an EEG machine, and PET scans to measure beta-amyloid deposits in their brains. The results revealed that individuals with high levels of beta-amyloid deposits with better deep sleep performed better on a memory test. 

This suggests that deep sleep acts as a cognitive reserve factor, blunting the effects of beta-amyloid pathology on memory. The study highlights the importance of non-REM slow-wave sleep in counteracting the memory-impairing effects of beta-amyloid deposits.

Deep, slow-wave sleep may act as a “life raft” that helps keep memory afloat, even in older adults with Alzheimer’s pathology, according to UC Berkeley researchers. The study analyzed the amount of beta-amyloid deposits in the brains of healthy participants and found that those who experienced higher levels of deep sleep had better memory retention than those who slept worse, compensating for the effects of the deposits.

While further research is needed, the study suggests that improved sleep hygiene could be an effective way to counteract some of the memory-impairing effects of Alzheimer’s.

In a study with 62 cognitively normal older adults, researchers used positron emission tomography (PET) scanning to measure beta-amyloid (Aβ) and sleep electroencephalography (EEG) recordings to quantify NREM SWA. They also had participants complete a face-name learning task that depended on the hippocampus.

The study found that deep sleep, specifically NREM slow-wave activity (SWA), helps to improve memory function in older adults with high levels of beta-amyloid deposits in their brains, which can be a risk factor for dementia. However, deep sleep did not have the same positive effect on memory function in those without beta-amyloid deposits. The researchers controlled for other factors that could affect memory function, and the results were still significant.

The study suggests that deep sleep (NREM SWA) is a new cognitive reserve factor that can protect against memory loss caused by a high AD pathology burden. This sleep function remained significant even after accounting for factors like education and physical activity, suggesting that sleep may be an independent cognitive reserve resource.

Unlike other cognitive reserve factors, sleep is modifiable, which means improving sleep may help preserve cognitive function against AD pathology both presently and in the future.

Journal Reference:

  1. Zavecz, Z., Shah, V.D., Murillo, O.G. et al. NREM sleep as a novel protective cognitive reserve factor in the face of Alzheimer’s disease pathology. BMC Medicine. DOI: 10.1186/s12916-023-02811-z
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