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Introduction IInsomnia with objective short sleep duration (OSSD) was found to be associated with higher risks of cardiometabolic disorders, and was therefore proposed to be a phenotype associated with higher physiological hyperarousal. Previous studies further reported that insomnia with OSSD had higher autonomic arousal as measured by heart rate variability (HRV) during sleep. Since sleep duration could be determined by the interplay of arousal and sleep drive and HRV during sleep could be influenced by sleep staging and quality, the present study examined the level of arousal and sleep drive prior to sleep with EEG power and HRV to further understand the phenotyping of insomnia. Methods Ninety-four insomnia patients participated in the study and went through one night of 8-hour PSG recording. They were divided, with a cut-off of PSG total sleep time of 6 hours, into two groups: an OSSD group (N=26; mean age=37.0 ±10.3; M:F=7:19; TST=286.21±87.21 min) and an objective normal sleep duration (ONSD) group (N=68, mean age=32.95 ±10.05, M:F=12: 56, TST=414.4±28.9 min). Resting-state EEG and EKG were recorded for a 6-min period, 3-min eye-opened (EO) with fixation focus and 3 mins eye-closed (EC), prior to bedtime. Results T-tests showed no significant difference in HRV measures (SDNN, RMSD, LF, HF, LF/HF) between the two groups, but shorter R-R interval for OSSD group than ONSD group. Mann-Whitney tests for EEG power showed significantly lower theta power at F3, F4, C3, C4, and O2, and higher sigma power at F3, C3, C4, O1, and O2 during EC, as well as lower theta power at C3 and higher sigma power at O2 during EO for OSSD group in comparison to ONSD group. Conclusion The results partially support that insomnia with OSSD is associated with physiological hyperarousal as indicated by faster heart rate and higher high frequency EEG power prior to sleep. However, the lower EEG theta power prior to sleep suggest that lower homeostatic sleep drive may also play a role for the insomnia with short objective sleep duration. Support (if any) Supported by Taiwan National Science and Technology Council

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)

Introduction Objective sleep duration has been suggested to be a novel biomarker in the phenotyping of insomnia (Vgontzas & Fernandez-Mendoza, 2013). It was hypothesized that insomnia phenotype with PSG-defined short sleep duration (< 6 hours) is associated with physiological hyperarousal, while the phenotype with normal sleep duration (≥ 6 hours), is associated with anxious-ruminative psychological profile and poor resources for coping with stress. The aim of this study was to assess whether these two insomnia phenotypes differ in terms of self-reported psychological and physiological features. Methods A total 45 (mean age=36.6, female=76%) insomnia patients underwent a polysomnographic evaluation, completed several self-rating scales (include ISI, BAI, BDI, FIRST, DBAS, and PSAS), and were split into two groups base on their objective sleep duration (cut-off 6 hours). Results When compared to the short sleep group using independent sample t-test, the normal sleep group showed a significant higher mean score on FIRST (t= -2.13; p< .05). The short sleep group showed non-significant trends to have higher mean scores on BDI and BAI. The scores on the other scales showed no significant differences between the two groups. The FIRST score correlated positively with the score of DBAS (r= 0.32; p< .05) and the total (r= 0.36; p< .05) and cognitive-subscale scores (r= 0.41; p< .01) on PSAS. The BAI score correlated positively with the score of the total (r= 0.53; p< .001) and somatic subscale (r= 0.59; p< .001) on PSAS. Conclusion These results support the hypotheses that the normal sleep phenotype tends to be more vulnerable to the impact of stress, especially on sleep, due to pre-sleep cognitive hyperarousal. Since the BAI scale contains more items regarding physiological symptoms of anxiety disorders, the tendency of higher BAI score in short sleep group may indicate that the short sleep phenotype has higher physiological arousal, which supports the phenotyping model proposed by Vgontzas and Fernandez-Mandoza. Support (if any)