Abstract
BackgroundClinical and pharmacological studies of obsessive-compulsive disorder (OCD) have suggested that the serotonergic systems are involved in the pathogenesis, while structural imaging studies have found some neuroanatomical abnormalities in OCD patients. In the etiopathogenesis of OCD, few studies have performed concurrent assessment of genetic and neuroanatomical variables.MethodsWe carried out a two-way ANOVA between a variable number of tandem repeat polymorphisms (5-HTTLPR) in the serotonin transporter gene and gray matter (GM) volumes in 40 OCD patients and 40 healthy controls (HCs).ResultsWe found that relative to the HCs, the OCD patients showed significant decreased GM volume in the right hippocampus, and increased GM volume in the left precentral gyrus. 5-HTTLPR polymorphism in OCD patients had a statistical tendency of stronger effects on the right frontal pole than those in HCs.ConclusionsOur results showed that the neuroanatomical changes of specific GM regions could be endophenotypes of 5-HTTLPR polymorphism in OCD.
Highlights
Clinical and pharmacological studies of obsessive-compulsive disorder (OCD) have suggested that the serotonergic systems are involved in the pathogenesis, while structural imaging studies have found some neuroanatomical abnormalities in Obsessive-compulsive disorder (OCD) patients
We found a significant difference between the OCD patients and healthy controls (HCs) in the distribution of LA allele carriers or non-LA allele carriers of 5-HTTLPR polymorphism a T test b Chi square test regarding illness duration, age of onset, total YaleBrown Obsessive Compulsive Scale (Y-BOCS), or the 17-item Hamilton Depression Rating Scale (HDRS) (Table 2)
We found a significant difference between the OCD patients and HCs in the distribution of LA allele carriers or non-LA allele carriers of 5-HTTLPR polymorphism (χ2=5.333, 1 df, P = 0.021; Table 1)
Summary
Clinical and pharmacological studies of obsessive-compulsive disorder (OCD) have suggested that the serotonergic systems are involved in the pathogenesis, while structural imaging studies have found some neuroanatomical abnormalities in OCD patients. In the etiopathogenesis of OCD, few studies have performed concurrent assessment of genetic and neuroanatomical variables. One of the reasons for this separation is that the biological bases of OCD and anxiety disorder are different [1]. Structural imaging studies have found neuroanatomical abnormalities in the cortico–striatal–thalamo–cortical (CSTC) circuits in OCD patients [2]. Positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) have revealed abnormal activities in different nodes of the CSTC circuits in OCD patients compared with healthy controls (HCs) [2, 5].
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