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Cross sectional analysis has shown an association between OSA severity and Aβ burden using amyloid-PET, globally and regionally in the precuneus among MCI patients. However, whether OSA accelerates longitudinal increases in Aβ burden in MCI patients is presently unclear.
Study participants included a total of 798 subjects with a diagnosis of MCI and were a subset of the ADNI cohort (adni.loni.usc.edu). OSA was self-reported and participants were labeled either as OSA+, or OSA−. Aβ burden was determined by florbetapir SUVRs calculated by averaging across the 4 cortical regions and dividing this cortical summary ROI by a composite reference region. Mean and variance of the Aβ data at each time point by OSA status were determined. To test whether OSA is associated with the rate of change in Aβ data longitudinally, SAS PROC MIXED was used to fit the model with randomly varying intercepts and slopes allowing dependence on OSA status. The final model was adjusted for sex, body mass index and CPAP use status since there was no difference between OSA groups for APOE e4 status, age and history of cardiovascular disease.
At baseline, there was significant variation between subjects in mean Aβ-42 volumes (intercept) (mean SUVR; B = 0.0008, Z-value =11.02, p < .0001). A significant variation in the change (slope) in Aβ-42 volumes over time was also seen (mean SUVR; B = 0.0084, Z-value =11.63, p < .0001). The covariance between the baseline Aβ-42 level and Aβ-42 volume change over time indicated that SDB subjects experienced a faster increase in brain Aβ-42 volumes over time (p < .0001). The rate of change in Aβ-42 deposition also varied significantly across OSA groups over the follow-up period.
Obstructive Sleep Apnea possibly facilitates longitudinal increases in amyloid burden in elderly Mild Cognitive Impairment individuals. Further research examining mechanisms underlying effects of OSA on the longitudinal increases in Aβ burden is needed.