Suppr超能文献

多能干细胞衍生神经元作为研究常染色体隐性帕金森病 (ARPD) 的体外模型:PLA2G6 和其他基因座。

Pluripotent Stem Cell Derived Neurons as In Vitro Models for Studying Autosomal Recessive Parkinson's Disease (ARPD): PLA2G6 and Other Gene Loci.

机构信息

National Centre for Biological Sciences, Tata Institute of Fundamental Research, Bengaluru, India.

出版信息

Adv Exp Med Biol. 2021;1347:115-133. doi: 10.1007/5584_2021_643.

Abstract

Parkinson's disease (PD) is a neurodegenerative motor disorder which is largely sporadic; however, some familial forms have been identified. Genetic PD can be inherited by autosomal, dominant or recessive mutations. While the dominant mutations mirror the prototype of PD with adult-onset and L-dopa-responsive cases, autosomal recessive PD (ARPD) exhibit atypical phenotypes with additional clinical manifestations. Young-onset PD is also very common with mutations in recessive gene loci. The main genes associated with ARPD are Parkin, PINK1, DJ-1, ATP13A2, FBXO7 and PLA2G6. Calcium dyshomeostasis is a mainstay in all types of PD, be it genetic or sporadic. Intriguingly, calcium imbalances manifesting as altered Store-Operated Calcium Entry (SOCE) is suggested in PLA2G6-linked PARK 14 PD. The common pathways underlying ARPD pathology, including mitochondrial abnormalities and autophagic dysfunction, can be investigated ex vivo using induced pluripotent stem cell (iPSC) technology and are discussed here. PD pathophysiology is not faithfully replicated by animal models, and, therefore, nigral dopaminergic neurons generated from iPSC serve as improved human cellular models. With no cure to date and treatments aiming at symptomatic relief, these in vitro models derived through midbrain floor-plate induction provide a platform to understand the molecular and biochemical pathways underlying PD etiology in a patient-specific manner.

摘要

帕金森病(PD)是一种主要为散发性的神经退行性运动障碍,但也有一些家族形式。遗传 PD 可以通过常染色体显性或隐性突变遗传。虽然显性突变与成人发病和 L-多巴反应性 PD 的原型相似,但常染色体隐性 PD(ARPD)则表现出非典型表型,并有额外的临床表现。年轻发病的 PD 也很常见,与隐性基因座的突变有关。与 ARPD 相关的主要基因有 Parkin、PINK1、DJ-1、ATP13A2、FBXO7 和 PLA2G6。钙代谢失衡是所有类型 PD 的主要特征,无论是遗传的还是散发性的。有趣的是,PLA2G6 相关的 PARK14 PD 中存在钙失衡,表现为改变的储存操作钙进入(SOCE)。ARPD 病理学的共同途径,包括线粒体异常和自噬功能障碍,可以使用诱导多能干细胞(iPSC)技术在体外进行研究,本文对此进行了讨论。目前尚无治愈方法,治疗方法也仅针对症状缓解,因此,源自 iPSC 的黑质多巴胺能神经元作为改进的人类细胞模型。由于动物模型不能真实复制 PD 病理生理学,因此通过中脑基板诱导产生的这些体外模型为以患者特异性方式理解 PD 病因的分子和生化途径提供了一个平台。

相似文献

8
Parkinson's disease: from genetics to treatments.帕金森病:从遗传学治疗。
Cell Transplant. 2013;22(4):639-52. doi: 10.3727/096368912X655082. Epub 2012 Oct 31.

本文引用的文献

8
Midbrain Organoids: A New Tool to Investigate Parkinson's Disease.中脑类器官:研究帕金森病的新工具。
Front Cell Dev Biol. 2020 May 19;8:359. doi: 10.3389/fcell.2020.00359. eCollection 2020.

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