0564 The mechanism of deficits in cognition of OSA: plasma amyloid-beta and tau protein level by the intervention design

Abstract Introduction Obstructive sleep apnea syndrome (OSAS) was shown to impair neurocognitive functioning, which was often attributed to hypoxia and sleep fragmentation. More recently, increased accumulation of amyloid-beta and tau protein in OSAS patients have gotten research attention and have been considered to be a possible cause of neurocognitive impairments. Positive airway pressure (PAP) treatment has been found to improve cognitive functioning in OSAS patients. The current study further explored the association of the effects of PAP treatment on neurocognitive and plasma amyloid-beta (Aβ) and tau protein levels. Methods Sixteen OSAS patients (M:F=10:6; age average = 53.35, SD = 10.43) participated in the study. A package of neurocognitive tasks (CPT-III, verbal paired association task, PASAT-R, and semantic verbal fluency) were administered and blood sample was collected both before and after a 3-month period of PAP intervention. The total tau and Aβ 42 levels in the patients’ plasma were quantified using an ultrasensitive immunomagnetic reduction assay. Results T-tests comparing cognitive performance before and after PAP treatment showed significant difference in total immediate recall score of verbal pair association task (t = 3.412, p = .002) and near significant differences in commission error on CPT-III (t = -.357, p = .097) and total score on PASAT-R (t = 1.35, p = .099). Other neurocognitive tasks as well as Aβ and tau proteins showed no significant changes. However, the change of Aβ after treatment correlated significantly with the improvement on the first immediate recall sequence (r = -.64, p = .005), and tau protein level correlated with the score on 2-sec-ISI subscale of PASAT-R (r = -.45, p = .048). Conclusion The present study showed that three months of PAP treatment was effective in improving immediate memory, but not in other cognitive functions or Aβ and tau protein levels. Moreover, some changes in memory and executive function were associated with decrease of Aβ and tau proteins. The preliminary results suggest that the neurocognitive impairment in OSAS patients might be partially associated with accumulation of Aβ and tau proteins. Future studies are needed to further confirm the findings. Support (if any)