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帕金森病伴淡漠患者的胆碱能基底前脑萎缩及皮质改变。

Cholinergic basal forebrain atrophy and cortical alterations in Parkinson's disease with apathy.

作者信息

Si Qianqian, Gan Caiting, Shan Aidi, Sun Huimin, Cao Xingyue, Ye Shiyi, Shi Jiaxin, Wan Chenhui, Wang Xufeng, Yuan Yongsheng, Zhang Kezhong

机构信息

Department of Neurology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, 210029, China.

Department of Neurology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, 210029, China.

出版信息

Parkinsonism Relat Disord. 2025 May;134:107793. doi: 10.1016/j.parkreldis.2025.107793. Epub 2025 Mar 13.

DOI:10.1016/j.parkreldis.2025.107793
PMID:40117894
Abstract

INTRODUCTION

Emerging evidences support the contribution of cholinergic deficiency to apathy in Parkinson's disease (PD). We aimed to ascertain the role of structural alterations of cholinergic basal forebrain (BF) and its innervated cortical regions in the pathogenesis of apathy in PD.

METHODS

Twenty-one PD patients with apathy (PD-A), 28 without apathy (PD-NA), and 20 healthy controls (HCs) were recruited in this study. Changes in subregional volumes of the BF were compared. Cortical thickness and local gyrification index (LGI) analysis were adopted to reveal the concomitant cortical alterations. The correlation with the severity of apathy and the diagnostic capacity were also assessed.

RESULTS

Compared to PD-NA and HCs groups, PD-A group showed excessively nucleus basalis of Meynert (NBM/Ch4) atrophy (p < 0.05 after Bonferroni correction), accompanied by cortical thinning and hypergyrification of the right entorhinal cortex (p < 0.001 after Bonferroni correction). Furthermore, regression analysis showing that the Ch4 volume was negatively associated with the severity of apathy in PD-A group (β = -23.198, T = -1.063, p = 0.039). All the above significant neuroimaging alterations showed good performance in identifying apathetic patients (p < 0.001).

CONCLUSION

Our findings highlighted that BF cholinergic degeneration driven by Ch4 atrophy may be involved in the pathogenesis of apathy in PD patients without dementia or depression.

摘要

引言

新出现的证据支持胆碱能缺乏对帕金森病(PD)冷漠症状的影响。我们旨在确定胆碱能基底前脑(BF)及其支配的皮质区域的结构改变在PD冷漠症状发病机制中的作用。

方法

本研究招募了21名患有冷漠症状的PD患者(PD-A)、28名无冷漠症状的PD患者(PD-NA)和20名健康对照者(HCs)。比较了BF各亚区域体积的变化。采用皮质厚度和局部脑回指数(LGI)分析来揭示伴随的皮质改变。还评估了与冷漠严重程度的相关性及诊断能力。

结果

与PD-NA组和HCs组相比,PD-A组显示Meynert基底核(NBM/Ch4)过度萎缩(经Bonferroni校正后p<0.05),同时伴有右侧内嗅皮质变薄和脑回增多(经Bonferroni校正后p<0.001)。此外,回归分析表明,PD-A组中Ch4体积与冷漠严重程度呈负相关(β=-23.198,T=-1.063,p=0.039)。上述所有显著的神经影像学改变在识别冷漠患者方面表现良好(p<0.001)。

结论

我们的研究结果强调,由Ch4萎缩驱动的BF胆碱能变性可能参与了无痴呆或抑郁的PD患者冷漠症状的发病机制。

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