Imaging Alzheimer pathology in late-life depression with PET and Pittsburgh compound-B
Imaging Alzheimer pathology in late-life depression with PET and Pittsburgh compound-B
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DOI：
10.1097/wad.0b013e31816c92bf
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发表时间：
2008-07-01
影响因子：
2.1
通讯作者：
Meltzer, Carolyn C.
中科院分区：
文献类型：
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作者：
Butters, Meryl A.;Klunk, William E.;Meltzer, Carolyn C.
越来越多的证据表明，老年抑郁症和阿尔茨海默病（AD）之间存在经验联系。AD的神经病理学，以前只在尸检中证实，现在可以在体内检测使用P-淀粉样蛋白的选择性成像配体。使用[C-11] 6-OH-BTA-1 [匹兹堡化合物-B（PiB）]进行的正电子发射断层扫描（PET）显示，在临床诊断为可能AD的患者中，皮质区的示踪剂保留较高，而在年龄匹配的对照组中，示踪剂保留较低。我们以前也报道过轻度认知功能障碍（MCI）患者的PiB保留可变。在这项研究中，我们使用PiB-PET来评估淀粉样蛋白是否存在于接受过治疗的老年抑郁症患者中，其中许多人有持续的认知障碍。我们评估了9例缓解的重性抑郁症受试者[3男6女，平均（SD）年龄= 71.8（5.7）岁]，9例抑郁症受试者中有7例也符合MCI的诊断标准。使用来自健康老年人[n = 8;平均（SD）年龄= 71.5（3.0）岁]的PiB-PET数据进行比较。通过动脉采样获取PET，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来量化PiB保留;动脉线路故障导致1名抑郁受试者被排除。数据表明PiB保留率显著升高。2名认知能力正常的抑郁症受试者的PiB保留在非抑郁症认知正常受试者的范围内。6例MCI抑郁症患者中有3例PiB保留在AD患者范围内。其余3例抑郁症伴MCI患者的PiB保留是可变的，通常介于其他受试者之间。我们的研究结果是一致的，并支持这一假设，即抑郁症可能预示着AD的发展，在一些人。
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 P-amyloid. Positron emission tomography (PET) with [C-11] 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.