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本文引用的文献

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Diagnostic accuracy of 18 F-FDG and 11 C-PIB-PET for prediction of short-term conversion to Alzheimer's disease in subjects with mild cognitive impairment.18 F-FDG 和 11 C-PIB-PET 对轻度认知障碍患者短期转化为阿尔茨海默病的预测诊断准确性。
Int J Clin Pract. 2012 Feb;66(2):185-98. doi: 10.1111/j.1742-1241.2011.02845.x.
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MDS Task Force on mild cognitive impairment in Parkinson's disease: critical review of PD-MCI.MDS 工作组关于帕金森病轻度认知障碍:对 PD-MCI 的批判性回顾。
Mov Disord. 2011 Aug 15;26(10):1814-24. doi: 10.1002/mds.23823. Epub 2011 Jun 9.
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Amyloid-dependent and amyloid-independent stages of Alzheimer disease.阿尔茨海默病的淀粉样蛋白依赖性和淀粉样蛋白非依赖性阶段。
Arch Neurol. 2011 Aug;68(8):1062-4. doi: 10.1001/archneurol.2011.70. Epub 2011 Apr 11.
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Amyloid precursor protein processing and Alzheimer's disease.淀粉样前体蛋白的加工与阿尔茨海默病。
Annu Rev Neurosci. 2011;34:185-204. doi: 10.1146/annurev-neuro-061010-113613.
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Amyloid-β associated cortical thinning in clinically normal elderly.临床正常老年人中与淀粉样蛋白-β相关的皮质变薄。
Ann Neurol. 2011 Jun;69(6):1032-42. doi: 10.1002/ana.22333. Epub 2011 Mar 17.
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Cerebrospinal fluid biomarkers for Parkinson disease diagnosis and progression.用于帕金森病诊断和进展的脑脊液生物标志物。
Ann Neurol. 2011 Mar;69(3):570-80. doi: 10.1002/ana.22311. Epub 2011 Mar 11.
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Apolipoprotein E in Alzheimer's disease and other neurological disorders.载脂蛋白 E 在阿尔茨海默病和其他神经紊乱中的作用。
Lancet Neurol. 2011 Mar;10(3):241-52. doi: 10.1016/S1474-4422(10)70325-2.
8
CSF Aβ(42) and tau in Parkinson's disease with cognitive impairment.帕金森病伴认知障碍患者的脑脊液 Aβ(42)和 tau。
Mov Disord. 2010 Nov 15;25(15):2682-5. doi: 10.1002/mds.23287.
9
CSF amyloid {beta} 1-42 predicts cognitive decline in Parkinson disease.脑脊液淀粉样蛋白β 1-42 可预测帕金森病的认知下降。
Neurology. 2010 Sep 21;75(12):1055-61. doi: 10.1212/WNL.0b013e3181f39a78. Epub 2010 Aug 18.
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Sharpen that needle.磨尖那根针。
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淀粉样蛋白与无痴呆的帕金森病患者的认知能力下降有关。

Amyloid is linked to cognitive decline in patients with Parkinson disease without dementia.

机构信息

Department of Neurology, Massachusetts General Hospital, Boston, USA.

出版信息

Neurology. 2013 Jan 1;80(1):85-91. doi: 10.1212/WNL.0b013e31827b1a07. Epub 2012 Dec 12.

DOI:10.1212/WNL.0b013e31827b1a07
PMID:23243071
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3589197/
Abstract

OBJECTIVE

To determine whether amyloid burden, as indexed by Pittsburgh compound B (PiB) retention, identifies patients with Parkinson disease with mild cognitive impairment (PD-MCI) compared to those with normal cognition (PD-nl). A related aim is to determine whether amyloid burden predicts cognitive decline in a cohort of subjects with PD without dementia.

METHODS

In this prospective cohort study, we examined 46 subjects with PD without dementia, of whom 35 had normal cognition and 11 met criteria for PD-MCI at study baseline. All subjects underwent standardized neurologic and neuropsychological examinations and PiB PET at baseline, and clinical examinations were conducted annually for up to 5 years.

RESULTS

At baseline, precuneus PiB retention did not distinguish PD-MCI from PD-nl. Subjects with PD-MCI declined more rapidly than PD-nl subjects on cognitive tests of memory, executive function, and activation retrieval. Of the 35 PD-nl subjects, 8 progressed to PD-MCI and 1 to dementia; of the 11 PD-MCI subjects, 5 converted to dementia. Both higher PiB retention and a diagnosis of PD-MCI predicted a greater hazard of conversion to a more severe diagnosis. Baseline PiB retention predicted worsening in executive function over time. The APOE ε4 allele also related to worsening in executive function, as well as visuospatial function, activation retrieval, and performance on the Mini-Mental State Examination. In contrast to its relation to cognitive decline, PiB retention did not affect progression of motor impairment.

CONCLUSIONS

At baseline measurements, amyloid burden does not distinguish between cognitively impaired and unimpaired subjects with PD without dementia, but our data suggest that amyloid contributes to cognitive, but not motor, decline over time.

摘要

目的

确定匹兹堡化合物 B(PiB)保留指数所代表的淀粉样蛋白负担是否可将帕金森病伴轻度认知障碍(PD-MCI)患者与认知正常(PD-nl)患者区分开来。相关目的是确定淀粉样蛋白负担是否可预测无痴呆帕金森病患者队列的认知下降。

方法

在这项前瞻性队列研究中,我们检查了 46 名无痴呆的帕金森病患者,其中 35 名认知正常,11 名符合 PD-MCI 的标准。所有患者在基线时接受了标准化的神经学和神经心理学检查以及 PiB PET,并且在长达 5 年的时间内每年进行临床检查。

结果

在基线时,扣带回后部的 PiB 保留并不能区分 PD-MCI 与 PD-nl。与 PD-nl 患者相比,PD-MCI 患者在记忆、执行功能和激活检索的认知测试中下降更快。在 35 名 PD-nl 患者中,有 8 名进展为 PD-MCI,1 名进展为痴呆;在 11 名 PD-MCI 患者中,有 5 名进展为痴呆。较高的 PiB 保留和 PD-MCI 的诊断均预测向更严重的诊断转变的风险更大。基线 PiB 保留可预测执行功能随时间的恶化。APOE ε4 等位基因也与执行功能以及视空间功能、激活检索和简易精神状态检查的表现恶化有关。与认知下降相反,PiB 保留不会影响运动功能的进展。

结论

在基线测量中,淀粉样蛋白负担不能区分无痴呆的帕金森病患者中认知受损和未受损的患者,但我们的数据表明,淀粉样蛋白随时间推移会导致认知而非运动功能下降。