Sleep homeostatic pressure and XXXX VNTR gene polymorphism influence antidepressant response to sleep @entity162 .

@entity1 @entity162 @entity1949 @entity308 @entity5395 @entity13076
BACKGROUND: Combined @entity1949 ( @entity1949 ) and light therapy (LT) cause a rapid improvement in @entity162 which has been hypothesized to be paralleled by changes in sleep homeostasis. Recent studies showed that @entity162 @entity1 had lower changes of EEG theta power after sleep and responders to antidepressant @entity1949 +LT slept less and showed a lower increase of EEG theta power then non-responders. A polymorphism in @entity5395 gene has been associated with diurnal preference, sleep structure and homeostatic response to sleep deprivation in healthy subjects. We hypothesized that the individual variability in the homeostatic response to @entity1949 could be a correlate of antidepressant response and be influenced by genetic factors. METHODS: We administered three @entity1949 +LT cycles to @entity162 @entity1 . Severity of @entity308 was rated on Hamilton Depression Rating Scale. Actigraphic recordings were performed in a group of @entity1 . RESULTS: @entity5395 polymorphism influenced changes in total sleep time (F=2.24; p=0.024): while @entity13076 ) and @entity5395 (4/5) @entity1 showed a reduction in it after treatment, @entity5395 (5/5) subjects showed an increase of about 40min, suggesting a higher homeostatic pressure. The same polymorphism influenced the change of depressive symptomatology during treatment (F=3.72; p=0.028). LIMITATIONS: Sleep information was recorded till the day after the end of treatment: a longer period of observation could give more information about the possible maintenance of allostatic adaptation. CONCLUSIONS: A higher sleep homeostatic pressure reduced the antidepressant response to @entity1949 +LT, while an allostatic adaptation to sleep loss was associated with better response. This process seems to be under genetic control.
