Major depressive disorder is a common mental disorders, the core symptoms of significant long-lasting low mood, decreased interest, anorgasmia. Depressive disorder lifetime prevalence rate of 12% - 17%, the heritability of 40% - 50%. At present, studies have shown that the protein kinase B1 (of AKT1) activity and depressive disorders.Depressive disorder often defects of cognitive function, particularly in the prefrontal executive dysfunction is the most prominent, and the damage is long-term. Based on this hypothesis, we assume that the AKT1 of functional changes related to changes in cognitive function may be associated with depressive disorders, to study the relevance of the cognitive function of AKT1 single nucleotide polymorphisms and major depressive disorder.
Major depressive disorder in patients with significant cognitive dysfunction, especially the prefrontal executive function impairment. Some scholars believe that depressive disorder is a cognitive process, barriers to the pathological basis of cognitive function disorders. Neurotrophic plasticity hypothesis of major depressive disorder, BDNF and its signaling pathway is a hot topic of the study, the conduction pathway genes will inevitably become the hot candidate gene for depressive disorder. AKT1 as a key gene in the BNDF P13-K pathway plays an important role in signal transduction. This study showed no significant correlation between the AKT1 gene polymorphism and major depressive disorder. Karege such as depressive disorder AKT1 activity confirmed the AKT1 association with depressive disorder. The findings were inconsistent and may be due to the study population, ethnic, the number of sample cases and disease heterogeneity.
Diverse clinical manifestations of major depressive disorder, phenotypic heterogeneity, different phenotypes may have different molecular genetic mechanisms. This study suggests that the AKT1 gene polymorphisms have varying degrees of cognitive function in major depressive disorder, G / G genotype in patients with cognitive dysfunction is more severe. The study found that the catechol-O-methyltransferase enzyme G allele and depressive disorder, cognitive function, especially executive function damage associated. COMT gene polymorphism may play a role in cognitive dysfunction in depressive disorders. The Rybakowski such as the use of small samples (44 cases of patients with bipolar depression) study found that BDNF-Va166Met gene polymorphism and cognitive function impair.