 Abstract Purpose of the study: To evaluate the effect of sertraline on polysomnographic PSG variables and clinical improvement in the treatment of depressive patients with insomnia. Methods used: The study design was 8-week and open-label trial. Patients were diagnosed as major depressive disorder. Their Hamilton Rating Scale for Depression HRSD score was more than 18, and HRSD-sleep disturbance score was more than 3. After 7-day wash-out period and 2 nights PSG the first night as adaptive and the second night as baseline, 31 depressive patients were administered by sertraline as 50 mg in 8 am in the 1st day. The dosage of sertraline would be titrated during the 8-week treatment, and the maximum was lower than 200 mgday. The primary endpoints were the changes of PSG variables from baseline to the 56th Day. The secondary endpoints were the changes of subjective sleep quality and clinical performance from baseline to the 56th Day. Their sleep quality was evaluated with Epworth Sleepiness Scale ESS and Pittsburgh Sleep Quality Index PSQI, and their clinical performance was evaluated with HRSD and Clinical Globe Impression CGI. Summary of results containing real data and appropriate statistical assessments: The Intent-to-Treat analysis included 31 subjects. The final dosage was titrated as 130.647.8 mgday. The Rapid Eye Movement REM sleep latency was prolonged significantly in the 1st day and throughout 8-week treatment. The percentage of REM sleep decreased significantly in the 1st day, but increased gradually along the following treatment. AI reached the highest level in the 1st day 13.87.2, and decreased along the following treatment. SL decreased significantly and reached normal range 30minutes after the visit of 14th day. The percentage of stage 3 increased gradually, and became higher in the 14th, 28th, 56th days. HRSD score was similar between baseline and the 1st day, and became significantly lower in the 14th, 28th, and 56th day. Similar pattern was shown in CGI. Scores of HRSD-sleep disturbance, PSQI, ESS decreased gradually throughout the treatment. The sleep latency in multiple sleep latency test maintained stable throughout treatment. The reducing score rates of HRSD and CGI-GI significantly correlated with the reducing score rate of REM latency in all visits, and they also significantly correlated with sleep latency, sleep efficiency, and stage 3 in some visits. Further, significant correlation was shown between the reducing score rate of HRSD in the 56th day and the the reducing score rate of REM latency in the 1st day r-0.733, P0.003. Conclusions: Sertraline was an effective antidepressant, and its effectiveness had relationship with the reduction of REM latency during the 8-week treatment. Further, the final clinical improvement could be predicted by the extent of shorten REM latency in the first night. So the suppression of REM sleep might be the key mechanism of antidepressive1. On the other hand, Sertraline had little alerting property without sleep disturbance in the treatment2. This property of sertraline must benefit the remission of depression, and the remission contributed the sleep improvement in turn. It was virtuous cycle in depressive treatment. 