Genetic pathway of major depressive disorder in shortening telomeric length

Context Shortened telomeric length has been associated with aging and monoamine oxidase A gene activity. The pathways of genetic activity and mental disorder in shortening telomeric length, however, remain unclear. Objective The purpose of this study was to explore the possible pathways of the monoamine oxidase A promoter, ApoE polymorphisms and telomeric length in major depressive disorder. Methods This study enrolled 253 unrelated patients with major depression in southern Taiwan, and was carried out between March 2001 and September 2004. In addition, 411 controls were randomly selected from the general population in southern Taiwan. Results Hierarchical regression showed that the influence of the monoamine oxidase A promoter and ApoE2 polymorphisms was not statistically significant to telomeric length, when additionally adjusting for major depressive disorder. A final robust structural equation model showed that aging and major depressive disorder both have a statistically significant shortening effect on telomeric length. Moreover, sex, the ApoE2 allele, and the monoamine oxidase A promoter polymorphism have indirect effects on telomeric length. Conclusion Major depressive disorder is a mediating factor between the monoamine oxidase A promoter polymorphism and telomeric length.