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Longitudinal degeneration of the basal forebrain predicts subsequent dementia in Parkinson's disease.
Neurobiology of Disease ( IF 5.1 ) Pub Date : 2020-03-05 , DOI: 10.1016/j.nbd.2020.104831
Joana B Pereira 1 , Sara Hall 2 , Mattis Jalakas 3 , Michel J Grothe 4 , Olof Strandberg 3 , Erik Stomrud 3 , Eric Westman 5 , Danielle van Westen 2 , Oskar Hansson 2
Affiliation  

Objectives

Cholinergic dysfunction plays a prominent role in cognitive impairment in Parkinson's disease (PD). The aim of this study was to assess the relationship of baseline and longitudinal basal forebrain atrophy with cognitive decline and dementia in PD.

Methods

We included 106 non-demented PD patients, 19 PD dementia (PDD) patients and 42 controls with longitudinal structural MRI and cognitive testing. After 4.2 ± 1.8 years, 20 non-demented PD patients were diagnosed with dementia (PD-dementia converters), whereas the rest of PD patients remained non-demented (stable-PD). We compared MRI volumes of the medial septum/diagonal band (Ch1/Ch2) and nucleus basalis of Meynert (Ch4) between groups. Cox regression analyses were applied to test whether Ch1/Ch2 or Ch4 atrophy could predict future dementia and linear mixed models assessed their association with cognitive decline.

Results

Compared to controls, we found reduced Ch4 baseline volumes in PD-dementia converters (p = .003) and those who already had PDD (p < .001) but not in stable-PD. Over time, there was a greater loss in Ch1/Ch2 volumes in PD-dementia converters and PDD compared to the other groups (p = .004). Baseline and longitudinal Ch4 volumes were associated with cognition (p < .002) and longitudinal Ch4 atrophy predicted future dementia (p = .009).

Conclusions

Atrophy of Ch4 precedes and predicts future dementia in PD and is followed by changes in Ch1/Ch2, reflecting a posterior-anterior pattern of basal forebrain atrophy. This pattern could be used to track the spread of cholinergic degeneration and identify patients at risk of developing dementia.



中文翻译:

基底前脑的纵向变性预示着帕金森氏病的继发性痴呆。

目标

胆碱能功能障碍在帕金森氏病(PD)的认知障碍中起重要作用。这项研究的目的是评估基线和基础基底前脑萎缩与PD认知下降和痴呆的关系。

方法

我们包括106例非痴呆的PD患者,19例PD痴呆(PDD)患者和42例具有纵向结构MRI和认知测试的对照。在4.2±1.8年后,有20位非痴呆的PD患者被诊断为痴呆症(PD-痴呆症转化者),而其余的PD患者则保持非痴呆(稳定PD)。我们比较了两组之间内侧隔/对角带(Ch1 / Ch2)和Meynert基底核(Ch4)的MRI体积。应用Cox回归分析测试Ch1 / Ch2或Ch4萎缩是否可以预测未来的痴呆,线性混合模型评估了它们与认知能力下降的关系。

结果

与对照组相比,我们发现PD-痴呆症转化者(p  = .003)和已经患有PDD(p  <.001)但不是稳定PD者的Ch4基线量减少。随着时间的推移,与其他组相比,PD痴呆症转化者和PDD中的Ch1 / Ch2体积损失更大(p  = .004)。基线和纵向Ch4量与认知能力相关(p  <.002),而纵向Ch4萎缩预测未来痴呆症(p  = .009)。

结论

Ch4萎缩先于并预测PD的痴呆症,随后Ch1 / Ch2发生变化,反映了基础前脑萎缩的前后模式。这种模式可用于追踪胆碱能退行性疾病的蔓延并确定有患痴呆症风险的患者。

更新日期:2020-03-05
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