Abstract
Recent studies have reported that methylation of the brain-derived neurotrophic factor (BDNF) gene promoter is associated with major depressive disorder (MDD). This study aimed to investigate the association between cortical thickness and methylation of BDNF promoters as well as serum BDNF levels in MDD. The participants consisted of 65 patients with recurrent MDD and 65 age- and gender-matched healthy controls. Methylation of BDNF promoters and cortical thickness were compared between the groups. The right medial orbitofrontal, right lingual, right lateral occipital, left lateral orbitofrontal, left pars triangularis, and left lingual cortices were thinner in patients with MDD than in healthy controls. Among the MDD group, right pericalcarine, right medical orbitofrontal, right rostral middle frontal, right postcentral, right inferior temporal, right cuneus, right precuneus, left frontal pole, left superior frontal, left superior temporal, left rostral middle frontal and left lingual cortices had inverse correlations with methylation of BDNF promoters. Higher levels of BDNF promoter methylation may be closely associated with the reduced cortical thickness among patients with MDD. Serum BDNF levels were significantly lower in MDD, and showed an inverse relationship with BDNF methylation only in healthy controls. Particularly the prefrontal and occipital cortices seem to indicate key regions in which BDNF methylation has a significant effect on structure.
Highlights
If brain-derived neurotrophic factor (BDNF) methylation influences the development and clinical course of MDD, the effects of this methylation may be reflected in brain structures
A study in rats suggested that Bdnf methylation resulted in decreased Bdnf mRNA expression in the prefrontal region[16]
We investigated the association between BDNF promoter methylation and cortical thickness among patients with recurrent MDD
Summary
If BDNF methylation influences the development and clinical course of MDD, the effects of this methylation may be reflected in brain structures. Methylation would inhibit expression of the BDNF gene, which in turn inhibits neurogenesis in cortex; because BDNF regulates neuronal survival, growth, immigration, axonal pruning, and dendritic growth[10] Epigenetic controls such as DNA methylation are considered a major mechanism by which neural plasticity is altered in response to various environmental stimuli in the mature neural system[11]. Since abnormal epigenetic regulation of the BDNF gene would result in neurodegenerative changes and decreased cortical thickness in patients with MDD, the relationship between the thinner cortices and BDNF promoter methylation in patients with MDD would likely have an inverse correlation. Recent studies have reported that first-episode patients with MDD might have increased volume in the cortical[18] and hippocampal[19] regions compared to healthy controls. To reliably examine the possible effects of BDNF promoter methylation on neurodegenerative changes as represented by cortical thickness, we recruited only patients with recurrent MDD
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