The Relationship between Parkin and Protein Aggregation in Neurodegenerative Diseases.

The Relationship between Parkin and Protein Aggregation in Neurodegenerative Diseases.
复制标题

DOI:
10.3389/fpsyt.2010.00015
复制
发表时间:
2010
影响因子:
4.7
通讯作者:
Moussa CE
Moussa CE
中科院分区:
医学3区
文献类型:
--
作者:
Khandelwal PJ;Moussa CE

文献摘要

被引文献

相似文献

神经退行性疾病中最显著的变化是蛋白质积聚和包涵体形成。包括阿尔茨海默病、突触核蛋白病和 tau蛋白病在内的几种神经退行性疾病具有一些重叠的临床症状,表现为帕金森症、认知能力下降和痴呆。随着疾病过程中退行性变的进展,临床症状表明存在汇聚的病理途径。从生物化学角度来看,蛋白质裂解、泛素化和磷酸化似乎在蛋白质聚集、包涵体形成和炎症反应中起着重要作用。接下来,我们概述了目前关于蛋白质积聚和星形胶质细胞增生作为神经退行性疾病的共同特征的知识,并对蛋白质降解和抗炎提出了见解。我们综述了E3 - 泛素连接酶以及帕金作为炎症迹象抑制剂和清除神经退行性疾病中淀粉样蛋白的策略的其他可能功能。
The most prominent changes in neurodegenerative diseases are protein accumulation and inclusion formation. Several neurodegenerative diseases, including Alzheimer's, the Synucleinopathies and Tauopathies share several overlapping clinical symptoms manifest in Parkinsonism, cognitive decline and dementia. As degeneration progresses in the disease process, clinical symptoms suggest convergent pathological pathways. Biochemically, protein cleavage, ubiquitination and phosphorylation seem to play fundamental roles in protein aggregation, inclusion formation and inflammatory responses. In the following we provide a synopsis of the current knowledge about protein accumulation and astrogliosis as a common denominator in neurodegenerative diseases, and we propose insights into protein degradation and anti-inflammation. We review the E3-ubiquitin ligase and other possible functions of parkin as a suppressant of inflammatory signs and a strategy to clear amyloid proteins in neurodegenerative diseases.