Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
Am J Geriatr Psychiatry. 2011 Jan;19(1):53-63. doi: 10.1097/jgp.0b013e3181eafde4.
Given the challenges in the clinical management of geriatric depression, research over the past decade has focused on developing early neurobiological markers of antidepressant treatment response. This study tested the hypothesis that lower baseline glucose metabolism and greater acute cerebral metabolic responses to a single, intravenous (IV) dose of the selective serotonin reuptake inhibitor (SSRI) citalopram would be associated with greater improvement of depressive symptoms after 12 weeks of citalopram treatment in geriatric depression.
sixteen geriatric depressed patients underwent two scans to measure cerebral glucose metabolism after administration of either a saline placebo or citalopram infusion (40 mg, IV). Then, the patients were treated with the oral citalopram medication for 12 weeks.
greater improvement of depressive symptoms was associated with lower baseline metabolism in anterior cingulate, superior, middle, and inferior frontal gyri (bilaterally), inferior parietal lobule (bilaterally), precuneus (right), insula (left), parahippocampal gyrus (right), caudate (bilaterally), and putamen (left) regions. Greater improvement of depressive symptoms was associated with greater reductions in metabolism after acute citalopram administration in similar brain regions, including additional posterior cortical regions.
lower baseline cerebral metabolism and greater decreases with acute citalopram administration are associated with better antidepressant response to chronic citalopram treatment. These data are consistent with previous studies of total sleep deprivation and suggest that dynamic, early adaptive changes or normalization of cerebral metabolism may represent early neurobiological markers of chronic SSRI treatment response in geriatric depression.
鉴于老年抑郁症临床管理的挑战，过去十年的研究重点是开发抗抑郁治疗反应的早期神经生物学标志物。本研究检验了以下假设，即较低的基线葡萄糖代谢和对选择性 5-羟色胺再摄取抑制剂（SSRI）西酞普兰单次静脉（IV）剂量的更大急性大脑代谢反应，与老年抑郁症患者接受西酞普兰治疗 12 周后抑郁症状的更大改善相关。
16 名老年抑郁症患者接受了两次扫描，以测量在给予生理盐水安慰剂或西酞普兰输注（40mg，IV）后大脑葡萄糖代谢。然后，患者接受西酞普兰口服药物治疗 12 周。
抑郁症状的更大改善与前扣带、额上、中、下回（双侧）、顶下小叶（双侧）、楔前叶（右侧）、岛叶（左侧）、海马旁回（右侧）、尾状核（双侧）和壳核（左侧）区域的基线代谢降低相关。抑郁症状的更大改善与急性西酞普兰给药后大脑相似区域代谢的更大降低相关，包括额外的皮质后区域。
较低的基线大脑代谢和急性西酞普兰给药后的更大降低与慢性西酞普兰治疗的更好抗抑郁反应相关。这些数据与之前关于总睡眠时间剥夺的研究一致，并表明大脑代谢的动态、早期适应性变化或正常化可能代表老年抑郁症慢性 SSRI 治疗反应的早期神经生物学标志物。
