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.