TY - JOUR
T1 - Insomnia improvement during antidepressant treatment and CLOCK gene polymorphism
AU - Serretti, Alessandro
AU - Cusin, Cristina
AU - Benedetti, Francesco
AU - Mandelli, Laura
AU - Pirovano, Adele
AU - Zanardi, Raffaella
AU - Colombo, Cristina
AU - Smeraldi, Enrico
PY - 2005/8/5
Y1 - 2005/8/5
N2 - Sleep disturbances are commonly observed in mood disorders, and sleep manipulations can influence the clinical status. In the present study, we investigated the possible effect of the 3111 T/C circadian locomotor output cycles kaput (CLOCK) gene polymorphism on insomnia symptomatology during antidepressant treatment. One hundred seventy-eight inpatients were treated with fluvoxamine 300 mg/day (n = 147) or paroxetine 20-40 mg/day (n = 31), and either placebo or pindolol in a double blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression (HAM-D). We observed a significantly higher presence of insomnia throughout the trial in homozygotes for the C variant (P = 0.026). Other demographic and clinical features were found not to be related with CLOCK polymorphisms. Overall, our findings may suggest that CLOCK genotype influences the time course of insomnia during antidepressant treatment. This, together with previous findings on this polymorphism could lead to a further dissection of the complexity of mood disorders.
AB - Sleep disturbances are commonly observed in mood disorders, and sleep manipulations can influence the clinical status. In the present study, we investigated the possible effect of the 3111 T/C circadian locomotor output cycles kaput (CLOCK) gene polymorphism on insomnia symptomatology during antidepressant treatment. One hundred seventy-eight inpatients were treated with fluvoxamine 300 mg/day (n = 147) or paroxetine 20-40 mg/day (n = 31), and either placebo or pindolol in a double blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression (HAM-D). We observed a significantly higher presence of insomnia throughout the trial in homozygotes for the C variant (P = 0.026). Other demographic and clinical features were found not to be related with CLOCK polymorphisms. Overall, our findings may suggest that CLOCK genotype influences the time course of insomnia during antidepressant treatment. This, together with previous findings on this polymorphism could lead to a further dissection of the complexity of mood disorders.
KW - Bipolar disorder
KW - Circadian rhythm
KW - CLOCK gene
KW - Insomnia
KW - Major depressive disorder
KW - Pharmacogenetics
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U2 - 10.1002/ajmg.b.30130
DO - 10.1002/ajmg.b.30130
M3 - Article
C2 - 15952199
AN - SCOPUS:23044441089
VL - 137 B
SP - 36
EP - 39
JO - American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics
JF - American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics
SN - 1552-4841
IS - 1
ER -