Suppr超能文献

对12例携带LRRK2 I2020T突变的家族性帕金森病患者进行神经病理学检查,包括tau蛋白和TDP - 43病理学检查。

Neuropathological examination of 12 cases of familial Parkinson's disease with LRRK2 I2020T mutation including tau and TDP-43 pathology.

作者信息

Uchino Akiko, Hasegawa Kazuko, Yagishita Saburo, Nagai Makiko, Ogino Mieko, Ogino Yutaka, Hatsuta Hiroyuki, Murayama Shigeo, Saito Yuko

机构信息

Department of Neuropathology (Brain Bank for Aging Research), Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Itabashi-ku, Tokyo, Japan.

Department of Preventive Medical Center, Kitasato University Kitasato Institute Hospital, Minato-ku, Tokyo, Japan.

出版信息

J Neurol. 2025 Jun 9;272(7):450. doi: 10.1007/s00415-025-13148-3.

Abstract

We previously reported a clinicopathological examination in the Sagamihara family, familial PD with LRRK I2020T mutation, highlighting the most common neuropathological finding as pure nigral degeneration without Lewy bodies (LBs). We applied immunohistochemical analysis to seven previously reported cases and evaluated five additional cases for a full neuropathological examination (altogether 12 cases). All cases exhibited nigral degeneration with a relatively preserved locus coeruleus (LC). Synuclein pathology was found in four cases, one of which showed multiple system atrophy pathology, and three showed LB pathology. Tau pathology in the brainstem mostly comprised a few neurofibrillary tangles and fell within the range of age-related changes. We found phosphorylated transactivation response element DNA-binding protein 43 kDa (pTDP-43) positive structures in five cases. Four of the five cases were observed in the substantia nigra (SN) but not limbic regions. The distribution pattern of pTDP-43 clearly differed from that in LB disease and older adults, suggesting that nigral degeneration is the primary lesion in the Sagamihara family. TDP-43 pathology in the Sagamihara family was different from those observed in TDP-43 proteinopathy that causes parkinsonism, which could be a secondary change; however, it may influence the course of the disease. Degeneration of the SN with relative preservation of the LC is a consistent finding in Sagamihara families, with or without LBs. These findings suggest that members of the Sagamihara family harbor a synuclein-independent neurodegenerative pathway and exhibit differential vulnerabilities depending on the brain region.

摘要

我们之前报道了相模原家族(伴有LRRK I2020T突变的家族性帕金森病)的临床病理检查,突出显示最常见的神经病理学发现为无路易小体(LB)的单纯黑质变性。我们对7例先前报道的病例进行了免疫组织化学分析,并评估了另外5例以进行全面的神经病理学检查(共12例)。所有病例均表现为黑质变性,蓝斑(LC)相对保留。在4例中发现了突触核蛋白病理学改变,其中1例显示多系统萎缩病理学改变,3例显示LB病理学改变。脑干中的tau病理学改变主要包括一些神经原纤维缠结,且在与年龄相关的变化范围内。我们在5例中发现了磷酸化的反式激活反应元件DNA结合蛋白43 kDa(pTDP-43)阳性结构。这5例中的4例在黑质(SN)中观察到,但在边缘区域未观察到。pTDP-43的分布模式明显不同于LB病和老年人中的分布模式,这表明黑质变性是相模原家族中的主要病变。相模原家族中的TDP-43病理学改变与在导致帕金森综合征的TDP-43蛋白病中观察到的不同,后者可能是一种继发性改变;然而,它可能会影响疾病进程。无论有无LB,黑质变性伴蓝斑相对保留是相模原家族中的一致发现。这些发现表明,相模原家族成员存在一条不依赖突触核蛋白的神经退行性通路,并且根据脑区表现出不同的易损性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/144e/12148971/4efa457c80c2/415_2025_13148_Fig1_HTML.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验