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β 三叶螺旋蛋白相关神经退行性疾病(BPAN)作为自噬缺陷导致的多方面神经病理学的一个遗传简单模型。

Beta-propeller protein-associated neurodegeneration (BPAN) as a genetically simple model of multifaceted neuropathology resulting from defects in autophagy.

机构信息

Neuroscience Academic Clinical Programme, Duke-NUS Medical School, Singapore 169857, Singapore.

Department of Research, National Neuroscience Institute, Singapore 308433, Singapore.

出版信息

Rev Neurosci. 2019 Apr 24;30(3):261-277. doi: 10.1515/revneuro-2018-0045.

Abstract

Autophagy is an essential and conserved cellular homeostatic process. Defects in the core and accessory components of the autophagic machinery would most severely impact terminally differentiated cells, such as neurons. The neurodevelopmental/neurodegenerative disorder β-propeller protein-associated neurodegeneration (BPAN) resulted from heterozygous or hemizygous germline mutations/pathogenic variant of the X chromosome gene WDR45, encoding WD40 repeat protein interacting with phosphoinositides 4 (WIPI4). This most recently identified subtype of the spectrum of neurodegeneration with brain iron accumulation diseases is characterized by a biphasic mode of disease manifestation and progression. The first phase involves early-onset of epileptic seizures, global developmental delay, intellectual disability and autistic syndrome. Subsequently, Parkinsonism and dystonia, as well as dementia, emerge in a subacute manner in adolescence or early adulthood. BPAN disease phenotypes are thus complex and linked to a wide range of other neuropathological disorders. WIPI4/WDR45 has an essential role in autophagy, acting as a phosphatidylinositol 3-phosphate binding effector that participates in autophagosome biogenesis and size control. Here, we discuss recent updates on WIPI4's mechanistic role in autophagy and link the neuropathological manifestations of BPAN's biphasic infantile onset (epilepsy, autism) and adolescent onset (dystonic, Parkinsonism, dementia) phenotypes to neurological consequences of autophagy impairment that are now known or emerging in many other neurodevelopmental and neurodegenerative disorders. As monogenic WDR45 mutations in BPAN result in a large spectrum of disease phenotypes that stem from autophagic dysfunctions, it could potentially serve as a simple and unique genetic model to investigate disease pathology and therapeutics for a wider range of neuropathological conditions with autophagy defects.

摘要

自噬是一种重要且保守的细胞内稳态过程。自噬机制的核心和辅助成分的缺陷将对终末分化细胞(如神经元)产生最严重的影响。神经发育/神经退行性疾病β-三叶螺旋蛋白相关神经退行性变(BPAN)是由 X 染色体基因 WDR45 的杂合或半合子种系突变/致病性变异引起的,该基因编码与磷酸肌醇 4 相互作用的 WD40 重复蛋白(WIPI4)。这种最近发现的具有脑铁积累疾病的神经退行性疾病谱的亚型的特征是疾病表现和进展的双相模式。第一阶段涉及早发性癫痫发作、全面发育迟缓、智力障碍和自闭症综合征。随后,帕金森病和肌张力障碍以及痴呆症以亚急性方式出现在青少年或成年早期。BPAN 疾病表型因此是复杂的,并与广泛的其他神经病理学疾病相关。WIPI4/WDR45 在自噬中具有重要作用,作为一种磷酸肌醇 3-磷酸结合效应物,参与自噬体的生物发生和大小控制。在这里,我们讨论了 WIPI4 在自噬中的机制作用的最新进展,并将 BPAN 的双相婴儿期发病(癫痫、自闭症)和青少年期发病(肌张力障碍、帕金森病、痴呆)表型的神经病理学表现与自噬损伤的神经后果联系起来,这些后果在许多其他神经发育和神经退行性疾病中已经或正在出现。由于 BPAN 中的单基因 WDR45 突变导致源自自噬功能障碍的广泛疾病表型,它可能潜在地作为一种简单而独特的遗传模型,用于研究具有自噬缺陷的更广泛神经病理学疾病的病理学和治疗方法。

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