Journal of Neuroinflammation | |
LRRK2 and neuroinflammation: partners in crime in Parkinson’s disease? | |
Elisa Greggio1  Luigi Bubacco1  Isabella Russo1  | |
[1] Department of Biology, University of Padova, Via Ugo Bassi 58/B, 35121 Pad ova, Italy | |
关键词: Dopaminergic neurons; Parkinson’s disease; Neurodegeneration; Microglia; Neuroinflammation; LRRK2; | |
Others : 811861 DOI : 10.1186/1742-2094-11-52 |
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received in 2013-12-31, accepted in 2014-02-25, 发布年份 2014 | |
【 摘 要 】
It is now well established that chronic inflammation is a prominent feature of several neurodegenerative disorders including Parkinson’s disease (PD). Growing evidence indicates that neuroinflammation can contribute greatly to dopaminergic neuron degeneration and progression of the disease. Recent literature highlights that leucine-rich repeat kinase 2 (LRRK2), a kinase mutated in both autosomal-dominantly inherited and sporadic PD cases, modulates inflammation in response to different pathological stimuli. In this review, we outline the state of the art of LRRK2 functions in microglia cells and in neuroinflammation. Furthermore, we discuss the potential role of LRRK2 in cytoskeleton remodeling and vesicle trafficking in microglia cells under physiological and pathological conditions. We also hypothesize that LRRK2 mutations might sensitize microglia cells toward a pro-inflammatory state, which in turn results in exacerbated inflammation with consequent neurodegeneration.
【 授权许可】
2014 Russo et al.; licensee BioMed Central Ltd.
【 预 览 】
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Figure 1.
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