Adding to a growing body of research associating sleep quality with the development of dementia and Alzheimer’s disease, a new study from the Washington University School of Medicine in St. Louis has homed in on the specific sleep phase that, when disrupted, can be linked to early stages of cognitive decline.

Sleep is important. That is something we know for sure. More recently a series of studies have been revealing compelling associations between disrupted sleep and neurodegenerative diseases such as Alzheimer’s. Last year it was discovered that sleep deprivation can directly lead to an increase in amyloid-beta accumulations in the brain, one of the central pathological observations seen in people with Alzheimer’s disease.

A new study is further elucidating the relationship between sleep and Alzheimer’s. The hypothesis behind the research is that decreased slow-wave sleep may correlate with increases in a brain protein called tau, which alongside amyloid-beta has been found to be significantly linked to the cognitive decline associated with Alzheimer’s disease.

The researchers examined the sleep patterns of 119 subjects over the age of 60, the majority of whom were cognitively healthy with no signs of dementia or Alzheimer’s. For a week the subjects’ sleep patterns were monitored using sensors and portable EEG monitors. Tau and amyloid levels were also tracked in all subjects using either PET scans or spinal fluid sampling.

The results revealed that those subjects suffering from lower levels of slow-wave sleep displayed higher volumes of tau protein in the brain. Slow-wave sleep is the deepest phase of non-rapid eye movement sleep and this stage of a person’s sleep cycle has been strongly linked to memory consolidation, with many researchers also suggesting slow-wave sleep is vital for maintaining general brain health.

“The key is that it wasn’t the total amount of sleep that was linked to tau, it was the slow-wave sleep, which reflects quality of sleep,” explains Brendan Lucey, first author on the new study. “The people with increased tau pathology were actually sleeping more at night and napping more in the day, but they weren’t getting as good quality sleep.”

Huge questions still remain unanswered though, particularly when trying to discern whether bad sleep is ultimately a cause, or consequence, of conditions such as Alzheimer’s. The study does clearly note a significant limitation in the conclusion is an inability to establish whether sleep changes precede, or follow, any pathological changes in the brain.

Age-related neurodegenerative diseases are inarguably more complicated than simply being the effect of years of bad sleep, however, the researchers do suggest sleep disruptions may be an effective early warning tool to help doctors spot patients in the earliest, pre-clinical stages of cognitive decline.

“What’s interesting is that we saw this inverse relationship between decreased slow-wave sleep and more tau protein in people who were either cognitively normal or very mildly impaired, meaning that reduced slow-wave activity may be a marker for the transition between normal and impaired,” says Lacey. “Measuring how people sleep may be a noninvasive way to screen for Alzheimer’s disease before or just as people begin to develop problems with memory and thinking.”

The new study was published in the journal Science Translational Medicine.

Source: Washington University School of Medicine in St. Louis

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