Butters Meryl A, Klunk William E, Mathis Chester A, Price Julie C, Ziolko Scott K, Hoge Jessica A, Tsopelas Nicholas D, Lopresti Brian J, Reynolds Charles F, DeKosky Steven T, Meltzer Carolyn C
Department of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, Pittsburgh, PA 15213, USA.
Alzheimer Dis Assoc Disord. 2008 Jul-Sep;22(3):261-8. doi: 10.1097/WAD.0b013e31816c92bf.
There is increasing evidence for an empiric link between late-life depression and Alzheimer disease (AD). The neuropathology of AD, previously only confirmed at autopsy, may now be detectable in vivo using selective imaging ligands for beta-amyloid. Positron emission tomography (PET) with [11C] 6-OH-BTA-1 [Pittsburgh Compound-B (PiB)] has shown high tracer retention in cortical areas in patients with clinical diagnoses of probable AD and low retention in age-matched controls. We also previously reported variable PiB retention in patients with mild cognitive impairment (MCI). In this study, we used PiB-PET to evaluate whether amyloid is present in elders with treated major depression, many of whom have persistent cognitive impairment. We evaluated 9 subjects with remitted major depression [3M: 6F, mean (SD) age=71.8(5.7) y]. Seven of the 9 depressed subjects also met criteria for the diagnosis of MCI. PiB-PET data from healthy elders [n=8; mean (SD) age=71.5(3.0) y] were used for comparison. PET was acquired with arterial sampling and PiB retention was quantified using magnetic resonance imaging-guided cortical regions and graphical analysis of time-activity data; arterial line failure led to exclusion of 1 depressed subject. The data demonstrated variably elevated PiB retention. PiB retention in the 2 depressed subjects with normal cognitive ability was in the range of nondepressed cognitively normal subjects. PiB retention in 3 of the 6 depressed subjects with MCI fell in the range of subjects with AD. PiB retention in the remaining 3 depressed subjects with cooccurring MCI was variable and generally was intermediate to the other subjects. Our findings are consistent with and supportive of the hypothesis that depression may herald the development of AD in some individuals.
越来越多的证据表明，老年期抑郁症与阿尔茨海默病（AD）之间存在经验性联系。AD的神经病理学以前只能在尸检时得到证实，现在可以使用针对β-淀粉样蛋白的选择性成像配体在体内进行检测。使用[11C]6-羟基-BTA-1[匹兹堡化合物-B（PiB）]进行正电子发射断层扫描（PET）显示，临床诊断为可能患有AD的患者在皮质区域的示踪剂保留率较高，而年龄匹配的对照组则保留率较低。我们之前还报道了轻度认知障碍（MCI）患者中PiB保留率的差异。在本研究中，我们使用PiB-PET来评估接受治疗的重度抑郁症老年人中是否存在淀粉样蛋白，其中许多人存在持续性认知障碍。我们评估了9名缓解期重度抑郁症患者[3名男性：6名女性，平均（标准差）年龄=71.8（5.7）岁]。9名抑郁症患者中有7名也符合MCI的诊断标准。来自健康老年人[n=8；平均（标准差）年龄=71.5（3.0）岁]的PiB-PET数据用于比较。通过动脉采样进行PET检查，并使用磁共振成像引导的皮质区域和时间-活动数据的图形分析对PiB保留率进行量化；动脉导管故障导致1名抑郁症患者被排除。数据显示PiB保留率有不同程度的升高。2名认知能力正常的抑郁症患者的PiB保留率处于非抑郁症认知正常受试者的范围内。6名患有MCI的抑郁症患者中有3名的PiB保留率处于AD患者的范围内。其余3名同时患有MCI的抑郁症患者的PiB保留率各不相同，总体上介于其他受试者之间。我们的研究结果与抑郁症可能预示着某些个体AD的发展这一假设一致，并支持该假设。
