Suppr超能文献

携带 PRKN 致病性变异的患者的下颌下腺中无 α-突触核蛋白病理学。

Negative α-synuclein pathology in the submandibular gland of patients carrying PRKN pathogenic variants.

机构信息

Department of Neurology, Seoul National University Hospital, Seoul National University, Seoul, South Korea.

Department of Pathology, Seoul National University Hospital, Seoul National University, Seoul, South Korea.

出版信息

Parkinsonism Relat Disord. 2020 Dec;81:179-182. doi: 10.1016/j.parkreldis.2020.07.004. Epub 2020 Jul 6.

Abstract

INTRODUCTION

Alpha-synuclein (AS) pathology in the peripheral nervous tissue is a potential pathological biomarker in Parkinson disease (PD). Several studies reported the excellent specificity of the AS pathology of the submandibular gland (SMG) biopsy in PD. PRKN pathogenic variant is one of the major genetic causes of young-onset PD without Lewy pathology in the brain. In this study, we evaluated peripheral AS pathology in the SMG biopsy of patients with PRKN pathogenic variants.

METHODS

We enrolled three young-onset PD patients with PRKN pathogenic variants. Two patients were compound heterozygous for trans-exon 3 and 4 deletions and one patient was heterozygous for an exon 2 duplication. We obtained two submandibular gland tissues with core needle biopsy (18G). The neural structures were identified using neurofilament (NF) immunostaining and the neural tissue in the adjacent section were stained with 129 phophorylated α-synuclein (pAS) antibody.

RESULTS

pAS staining in the SMG was negative in all cases with the PRKN pathogenic variants.

CONCLUSIONS

Our data may support the high specificity of the AS pathology of SMG in α-synuclein associated parkinsonism. Future studies evaluating peripheral neural tissue including the SMG in the elderly healthy population are required to validate the role of peripheral AS pathology as a biomarker in PD.

摘要

简介

α-突触核蛋白(AS)在周围神经组织中的病理学改变是帕金森病(PD)的一种潜在的病理学生物标志物。多项研究报道了下颌下腺(SMG)活检中 AS 病理学改变在 PD 中的优异特异性。PRKN 致病性变异是一种主要的遗传原因,导致年轻发病且无脑内路易体病理的 PD。在这项研究中,我们评估了 PRKN 致病性变异患者的 SMG 活检中的外周 AS 病理学改变。

方法

我们纳入了三名 PRKN 致病性变异的年轻发病 PD 患者。两名患者为跨外显子 3 和 4 缺失的复合杂合子,一名患者为外显子 2 重复的杂合子。我们使用 18G 芯针活检获得了两个下颌下腺组织。使用神经丝(NF)免疫染色识别神经结构,并用 129 磷酸化α-突触核蛋白(pAS)抗体对相邻切片中的神经组织进行染色。

结果

所有 PRKN 致病性变异患者的 SMG 中 pAS 染色均为阴性。

结论

我们的数据可能支持 SMG 中 AS 病理学改变在与α-突触核蛋白相关的帕金森病中的高特异性。需要进一步评估包括老年人健康人群的 SMG 在内的外周神经组织,以验证外周 AS 病理学改变作为 PD 生物标志物的作用。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验