PET Reveals Lack of Sleep as Alzheimer’s Risk Factor

The amount of sleep older adults get can directly impact their risk of Alzheimer’s, according to newly published imaging findings.

Revealed with PET scans, older individuals with mild cognitive impairment who sleep less than six hours nightly have more accumulation of amyloid – an identified contributing factor to Alzheimer’s disease – than do people who sleep more. This study, conducted by researchers from Japan, was published June 9 in JAMA Open.

To date, existing research has identified several lifestyle factors that can contribute to Alzheimer’s risk in older adults. But, this team, led by Noriyuki Kimura, Ph.D., from Oita University in Japan, elected to exam the effects of these factors, including steps walked, conversation time, and sleep hours, simultaneously. It is the first study to point to the lack of sleep as a modifiable risk factor for dementia in adults who already have mild cognitive impairment, they said.

“The present study is the first to clarify the association of various lifestyle factors with PET imaging simultaneously in older adults with [mild cognitive impairment],” Kimura’s team wrote. “Our results provide novel and interesting insights into the mechanisms underlying the association between lifestyle factors and cortical amyloid burden or brain function in older adults with [mild cognitive impairment.]”

It is possible, the team said, that these findings could contribute to novel evidence-based interventions that could potentially delay cognitive impairment in older adults.

To make this determination, Kimura’s team gathered and examined lifestyle data from 855 adults over age 65. Using a standardized cognitive function test, investigators identified 118 adults (13.8 percent) who already had mild cognitive impairment. This group was given wristband sensors to be worn all day, except while bathing, to collect data on walking steps, conversation time, and the specifics of their sleep quality, including total time asleep, sleep efficiency, and time awake after the onset of sleep. Study participants also underwent PET scans using two radiopharmaceuticals – carbon-11-labeled Pittsburgh compound B (PiB) and fluorine-18 FDG – to pinpoint the accumulated level of amyloid in the brain.

According to their analysis, researchers determined PiB uptake was lower in participants who got more than 325 minutes of sleep. Additionally, the FDG uptake among these same individuals pointed to higher glucose metabolism. However, investigators did not see any statistically significant associations between PiB or FDG uptake and walking steps, conversation time, and sleep efficiency.

The most interesting study finding, they pointed out, was the inverse relationship between total sleep time and cerebral glucose metabolism. According to existing research, they said, beta amyloid accumulates in the brain during time spent awake and can be cleared from the brain more effectively during sleep. Other studies have also revealed that a lack of sleep promotes beta amyloid production while simultaneously slowing down how quickly it is cleared, leading to the build-up of plaque in the brain.

These study findings, coupled with their own, they said, point to the critical nature of sleep duration as a modifiable Alzheimer’s risk factor.

“These results lead us to hypothesize that sleep duration may be an important lifestyle factor associated with cortical amyloid burden and brain function,” they concluded.