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LRRK2 and neuroinflammation: partners in crime in Parkinson's disease?

期刊

JOURNAL OF NEUROINFLAMMATION
卷 11, 期 -, 页码 -

出版社

BMC
DOI: 10.1186/1742-2094-11-52

关键词

LRRK2; Neuroinflammation; Microglia; Neurodegeneration; Parkinson's disease; Dopaminergic neurons

资金

  1. Michael J. Fox Foundation for Parkinson's Disease
  2. Italian Ministry of University and Research (Rientro dei Cervelli, lncentivazione alla mobilita di studiosi stranieri e italiani residenti all'estero)
  3. CARIPLO Foundation [2011-0540]
  4. Telethon - Italy [GGP12237]

向作者/读者索取更多资源

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.

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