JOURNAL ARTICLE

Serotonin transporter polymorphisms, microstructural white matter abnormalities and remission of geriatric depression

George S Alexopoulos, Christopher F Murphy, Faith M Gunning-Dixon, Charles E Glatt, Vassilios Latoussakis, Robert E Kelly, Dora Kanellopoulos, Sibel Klimstra, Kelvin O Lim, Robert C Young, Matthew J Hoptman
Journal of Affective Disorders 2009, 119 (1-3): 132-41
19375170

OBJECTIVE: This study compared microstructural abnormalities in depressed elders and controls and studied the association of the serotonin transporter gene status to white matter abnormalities and to remission of depression.

METHODS: The subjects were Caucasians with non-psychotic major depression and normal elders. Depressed subjects received escitalopram 10 mg daily for 12 weeks. Remission was defined as a HDRS score of 7 or below for 2 consecutive weeks. Diffusion tensor imaging was performed and voxel-based analysis of fractional anisotropy (FA) was conducted using age and mean diffusivity as covariates.

RESULTS: Depressed elders (N=27) had lower FA than controls (N=27) in several frontolimbic areas. Depressed elderly S-allele carriers also had lower FA than L homozygotes in frontolimbic brain areas, including the dorsal and rostral anterior cingulate, posterior cingulate, dorsolateral prefrontal and medial prefrontal regions, thalamus, and in other regions. S-allele carriers had a lower remission rate than L homozygotes.

LIMITATIONS: Small number of subjects, lack of random sampling, fixed antidepressant dose, short follow-up.

CONCLUSIONS: Lower FA was observed in several frontolimbic and other regions in depressed elders compared to controls. Depressed S-allele carriers had both microstructural white matter abnormalities in frontolimbic networks and a low remission rate. It remains unclear whether the risk for chronicity of geriatric depression in S-allele carriers is mediated by frontolimbic compromise. However, these observations set the stage for studies aiming to identify the relationship of S allele to impairment in specific frontolimbic functions interfering with response of geriatric depression to antidepressants.

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