INFLAMMATION IS GENETICALLY IMPLICATED IN PARKINSON'S DISEASE

被引:159
|
作者
Dzamko, N. [1 ,2 ]
Geczy, C. L. [1 ]
Halliday, G. M. [1 ,2 ]
机构
[1] Univ New S Wales, Sch Med Sci, Sydney, NSW 2052, Australia
[2] Neurosci Res Australia, Randwick, NSW 2031, Australia
基金
英国医学研究理事会;
关键词
TLR; innate; LRRK2; synuclein; inflammation; parkin; NECROSIS-FACTOR-ALPHA; NEURONOPATHIC GAUCHER-DISEASE; GENOME-WIDE ASSOCIATION; BLOOD MONONUCLEAR-CELLS; INCREASED SERUM-LEVELS; KINASE; INHIBITORS; CEREBROSPINAL-FLUID; TNF-ALPHA; MITOCHONDRIAL DYSFUNCTION; MOUSE MODEL;
D O I
10.1016/j.neuroscience.2014.10.028
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Inflammation has long been associated with the pathogenesis of Parkinson's disease (PD) but the extent to which it is a cause or consequence is sill debated. Over the past decade a number of genes have been implicated in PD. Relatively rare missense mutations in genes such as LRRK2, Parkin, SNCA and PINK1 are causative for familial PD whereas more common variation in genes, including LRRK2, SNCA and GBA, comprise risk factors for sporadic PD. Determining how the function of these genes and the proteins they encode are altered in PD has become a priority, as results will likely provide much needed insights into contributing causes. Accumulating evidence indicates that many of these genes function in pathways that regulate aspects of immunity, particularly inflammation, suggesting close associations between PD and immune homeostasis. (C) 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:89 / 102
页数:14
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