Dugger Brittany N, Serrano Geidy E, Sue Lucia I, Walker Douglas G, Adler Charles H, Shill Holly A, Sabbagh Marwan N, Caviness John N, Hidalgo Jose, Saxon-Labelle Megan, Chiarolanza Glenn, Mariner Monica, Henry-Watson Jonette, Beach Thomas G
Banner Sun Health Research Institute, Sun City, AZ.
J Parkinsons Dis. 2012 Jan 1;2(1):57-65. doi: 10.3233/JPD-2012-11073.
Dementia is a frequent complication of Parkinson's disease (PD). About half of PD dementia (PDD) is hypothesized to be due to progression of the underlying Lewy body pathology into limbic regions and the cerebral cortex while the other half is thought to be due to coexistent Alzheimer's disease. Clinically, however, these are indistinguishable. The spread of amyloid plaques to the striatum has been reported to be a sensitive and specific indicator of dementia due to Alzheimer's disease (AD). The purpose of the present study was to determine if the presence of striatal plaques might also be a useful indicator of the presence of diagnostic levels of AD pathology within PD subjects. We analyzed neuropathologically-confirmed cases of PD without dementia (PDND, N = 31), PDD without AD (PDD, N = 31) and PD with dementia meeting clinicopathological criteria for AD (PDAD, N =40). The minimum diagnostic criterion for AD was defined as including a clinical history of dementia, moderate or frequent CERAD cortical neuritic plaque density and Braak neurofibrillary stage III-VI. Striatal amyloid plaque densities were determined using Campbell-Switzer and Thioflavine S stains. Striatal plaque densities were significantly higher in PDAD compared to PDD (p<0.001). The presence of striatal plaques was approximately 80% sensitive and 80% specific for predicting AD. In comparison, the presence of cerebral cortex plaques alone was highly sensitive (100%) but had poor specificity (48% to 55%). The results suggest that striatal amyloid imaging may be clinically useful for making the distinction between PDD and PDAD.
痴呆是帕金森病（PD）常见的并发症。据推测，约一半的帕金森病痴呆（PDD）是由于潜在的路易体病理进展至边缘系统和大脑皮层，而另一半则被认为是由于并存的阿尔茨海默病。然而，在临床上，这两者难以区分。据报道，淀粉样斑块扩散至纹状体是阿尔茨海默病（AD）所致痴呆的敏感且特异的指标。本研究的目的是确定纹状体斑块的存在是否也可能是PD患者中AD病理诊断水平存在的有用指标。我们对经神经病理学确诊的无痴呆帕金森病（PDND，N = 31）、无AD的PDD（PDD，N = 31）以及符合AD临床病理标准的伴痴呆帕金森病（PDAD，N = 40）病例进行了分析。AD的最低诊断标准定义为包括痴呆的临床病史以及中度或频繁的CERAD皮质神经炎性斑块密度和Braak神经纤维缠结分期III - VI。使用Campbell - Switzer和硫黄素S染色来确定纹状体淀粉样斑块密度。与PDD相比，PDAD的纹状体斑块密度显著更高（p<0.001）。纹状体斑块的存在对预测AD的敏感性约为80%，特异性约为80%。相比之下，仅大脑皮层斑块的存在敏感性很高（100%），但特异性较差（48%至55%）。结果表明，纹状体淀粉样成像在临床上可能有助于区分PDD和PDAD。
