Serotonin transporter polymorphisms, microstructural white matter abnormalities and remission of geriatric depression.
Serotonin transporter polymorphisms, microstructural white matter abnormalities and remission of geriatric depression.
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DOI：
10.1016/j.jad.2009.03.004
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发表时间：
2009-12
影响因子：
6.6
通讯作者：
Hoptman, Matthew J.
中科院分区：
文献类型：
--
作者：
Alexopoulos, George S.;Murphy, Christopher F.;Gunning-Dixon, Faith M.;Glatt, Charles E.;Latoussakis, Vassilios;Kelly, Robert E., Jr.;Kanellopoulos, Dora;Klimstra, Sibel;Lim, Kelvin O.;Young, Robert C.;Hoptman, Matthew J.
目的本研究比较了抑郁老年人和对照者的微观结构异常，并研究了血清素转运蛋白基因状态与白质异常和抑郁缓解的关系。方法研究对象为患有非精神病性重度抑郁症的白人和正常老年人。抑郁症受试者每天接受 10 毫克艾司西酞普兰治疗，持续 12 周。缓解定义为连续 2 周 HDRS 评分为 7 或以下。进行扩散张量成像，并使用年龄和平均扩散率作为协变量进行基于体素的分数各向异性 (FA) 分析。 结果 抑郁老年人 (N=27) 在几个额边缘区域的 FA 低于对照组 (N=27)。抑郁的老年S等位基因携带者在额边缘脑区域的FA也低于L纯合子，这些区域包括背侧和喙侧前扣带回、后扣带回、背外侧前额叶和内侧前额叶区域、丘脑和其他区域。 S等位基因携带者的缓解率低于L纯合子。局限性受试者数量少、缺乏随机抽样、固定抗抑郁剂量、随访时间短。结论与对照相比，在抑郁老年人的几个额边缘和其他区域观察到FA较低。抑郁的 S 等位基因携带者在额边缘网络中存在微结构白质异常，并且缓解率较低。目前尚不清楚 S 等位基因携带者慢性老年抑郁症的风险是否是由额边缘损害介导的。然而，这些观察结果为旨在确定 S 等位基因与特定额边缘功能损伤（干扰老年抑郁症抗抑郁药反应）之间关系的研究奠定了基础。
OBJECTIVEThis 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.METHODSThe 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.RESULTSDepressed 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.LIMITATIONSSmall number of subjects, lack of random sampling, fixed antidepressant dose, short follow-up.CONCLUSIONSLower 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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影响因子：
10.6
作者：
Drevets, WC
通讯作者：
Drevets, WC
影响因子：
11.2
作者：
Cushman, Mary;Cantrell, Ronald A.;McClure, Leslie A.;Howard, George;Prineas, Ronald J.;Moy, Claudia S.;Temple, Ella M.;Howard, Virginia J.
通讯作者：
Howard, Virginia J.
影响因子：
17.7
作者：
Alexopoulos, George S.;Murphy, Christopher F.;Hoptman, Matthew J.
通讯作者：
Hoptman, Matthew J.
影响因子：
10.4
作者：
Abdelmalik, N.;Ruhe, H. G.;Kamphuisen, P. W.
通讯作者：
Kamphuisen, P. W.
DOI：
10.2165/00129785-200303020-00007
发表时间：
2003-01-01
期刊：
American journal of pharmacogenomics : genomics-related research in drug development and clinical practice
影响因子：
--
作者：
Lotrich, Francis E;Pollock, Bruce G;Ferrell, Robert E
通讯作者：
Ferrell, Robert E