Alzheimer’s Biomarker Tied to Sleep Apnea



PHILADELPHIA -- Sleep apnea was tied to higher tau protein burden in the entorhinal cortex, a preliminary cross-sectional study showed.

As measured in PET scans, older adults with apnea had significantly higher levels of tau in the entorhinal cortex on average than those who did not have apnea, after controlling for age, sex, education, cardiovascular risk, and other factors, reported Diego Carvalho, MD, of the Mayo Clinic in Rochester, Minnesota, and colleagues, in an early-release abstract from the American Academy of Neurology meeting to be held here in May.

The findings come on the heels of other studies of sleep and tau, including research from Washington University in St. Louis that showed non-REM slow wave activity was tied to tau pathology: people with increased tau pathology were sleeping more, but were not getting good quality sleep.

Previous studies also found that increased napping was associated with increased amyloid beta accumulation over time, and that decreased non-REM slow waves correlated with increased amyloid beta burden in the medial prefrontal cortex.

In the current study, investigators identified 288 cognitively unimpaired people age 65 and older from the Mayo Clinic Study of Aging who had both tau PET and amyloid PET scans. The cohort included people whose bed partners had completed a questionnaire assessing whether they had witnessed episodes of stopped breathing during sleep.

In the PET data, the researchers selected the entorhinal cortex as their region of interest because it is highly susceptible to tau accumulation, and used the cerebellum crus as a reference region to calculate a standardized uptake value ratio (SUVR).

Apnea was witnessed in 43 participants (15%). Witnessed apnea was significantly associated with tau burden in the entorhinal cortex, with the researchers estimating a 0.049-point elevation (95% CI 0.011-0.087, P=0.012) in the entorhinal cortex tau SUVR, after controlling for multiple confounders. In an email, Carvalho told MedPage Today that participants with apnea showed a 4.5% greater tau burden in the entorhinal cortex compared with non-apnea participants.

The study was limited by its relatively small sample size and preliminary nature, he added. It also did not include sleep studies to confirm the presence and severity of sleep apnea and lacked information about whether participants were receiving apnea treatment.

"Our research results raise the possibility that sleep apnea affects tau accumulation," Carvalho said in a statement. "But it's also possible that higher levels of tau in other regions may predispose a person to sleep apnea, so longer studies are now needed to solve this chicken-and-egg problem."

This study was supported by the NIH/NIA.

Source: https://www.medpagetoday.com/meetingcoverage/aan/78313

Obstructive, sleep, apnea and Longitudinal



Obstructive sleep apnea is associated with early but possibly modifiable Alzheimer's disease as U.S. Measles Outbreaks Spread, Why Does ’Anti-Vax’ Movement Persist? biomarkers changes. He hopes future research will tackle those and other questions. "This finding is important because it means we could potentially treat sleep problems to reduce risk of AD years down the road.". The study dangerous Bacteria May Lurk in Hospital Sinks was not able to answer the role of sleep stages, the extent of the damage that poor sleep might cause, nor "the extent to which treatment of OSA (obstructive sleep apnea) or other disorders or increased sleep duration. "Several studies have suggested that sleep disturbances might contribute to amyloid deposits and accelerate cognitive decline in those at risk for AD said Ricardo. "We know that sleep is necessary to clear toxins and beta-amyloid in the brain said study author. Treatment for...

Obstructive sleep apnea (OSA) may put elderly people at greater risk of developing Alzheimer's disease (AD according to new research published online in the American Thoracic Society's. Conclusions: We hypothesize that OSA reducing sleep quality and producing intermittent hypoxia lowers CSF A42 levels, increases CSF lactate levels, and alters cognitive performances in SCI patients, thus inducing early AD clinical and neuropathological biomarkers changes. But according to the US Centers for Disease Control and Prevention, one in three Americans don't get enough sleep. If sleep is disrupted, it can become easier for these proteins to gather. Osorio, MD, senior study author and assistant professor of psychiatry at New York University School of Medicine. What the study revealed, prashanthi Vemuri, PhD, an associate professor of radiology in the Alzheimers Disease Research Center at the Mayo Clinic, is one of the co-authors of the study.