Recent advances in the mechanisms of neuroinflammation and their roles in neurodegeneration. (November 2018)
- Record Type:
- Journal Article
- Title:
- Recent advances in the mechanisms of neuroinflammation and their roles in neurodegeneration. (November 2018)
- Main Title:
- Recent advances in the mechanisms of neuroinflammation and their roles in neurodegeneration
- Authors:
- Niranjan, Rituraj
- Abstract:
- Abstract: Neuroinflammation is associated with the pathogenesis of many neurological disorders including Parkinson's disease, Alzheimer's disease, Amyotrophic lateral sclerosis and Huntington disease. Current studies in this area have advanced the mechanism of neuroinflammation and its role in neurodegeneration. Studies from epidemiologic, clinical and animal models also contributed in the various new mechanisms of neuroinflammation. In this line, activation of monocytes is an important emerging mechanism that has a, profound role in neuroinflammation and neurodegeneration. Ion channels, matrix metalloproteases and microRNAs are also found to be the key players in the pathogenesis of neuroinflammation. In particular, microRNA-32 regulates microglia-mediated neuroinflammation and thus neurodegeneration. Notably, some important studies describe the role of Th17 cells in neuroinflammation, but, very little knowledge is available about their mechanism of action. Particularly, the role of autophagy gets emphasized, which plays a very critical role in protein aggregation and neurodegeneration. In this review, we highlight and discuss the mechanisms of these mediators of inflammation by which they contribute to the disease progression. In conclusion, we focus on the various newer molecular mechanisms that are associated with the basic understanding of neuroinflammation in neurodegeneration. Highlights: Monocytes activation is an emerging mechanism with a profound role inAbstract: Neuroinflammation is associated with the pathogenesis of many neurological disorders including Parkinson's disease, Alzheimer's disease, Amyotrophic lateral sclerosis and Huntington disease. Current studies in this area have advanced the mechanism of neuroinflammation and its role in neurodegeneration. Studies from epidemiologic, clinical and animal models also contributed in the various new mechanisms of neuroinflammation. In this line, activation of monocytes is an important emerging mechanism that has a, profound role in neuroinflammation and neurodegeneration. Ion channels, matrix metalloproteases and microRNAs are also found to be the key players in the pathogenesis of neuroinflammation. In particular, microRNA-32 regulates microglia-mediated neuroinflammation and thus neurodegeneration. Notably, some important studies describe the role of Th17 cells in neuroinflammation, but, very little knowledge is available about their mechanism of action. Particularly, the role of autophagy gets emphasized, which plays a very critical role in protein aggregation and neurodegeneration. In this review, we highlight and discuss the mechanisms of these mediators of inflammation by which they contribute to the disease progression. In conclusion, we focus on the various newer molecular mechanisms that are associated with the basic understanding of neuroinflammation in neurodegeneration. Highlights: Monocytes activation is an emerging mechanism with a profound role in neuroinflammation. The ion channels, matrix metaloproteases (MMPs), microRNAs are new key players in the pathogenesis of neuroinflammation. The roles of Th-17 cells and autophagy-mediated protein aggregation are new concepts in neuroinflammation-associated neurodegeneration. … (more)
- Is Part Of:
- Neurochemistry international. Volume 120(2018)
- Journal:
- Neurochemistry international
- Issue:
- Volume 120(2018)
- Issue Display:
- Volume 120, Issue 2018 (2018)
- Year:
- 2018
- Volume:
- 120
- Issue:
- 2018
- Issue Sort Value:
- 2018-0120-2018-0000
- Page Start:
- 13
- Page End:
- 20
- Publication Date:
- 2018-11
- Subjects:
- Neuroinflammation -- Monocytes and T cells -- Inflammatory mediators -- Matrix mettaloproteinases -- Autophagy
ASIC acid-sensing ion channels -- ALS amyotrophic lateral sclerosis -- MMPs matrix metalloproteases -- PD Parkinson's disease -- AD Alzheimer's Disease -- ROS reactive oxygen species -- RNS reactive nitrogen species -- TNF-α tumor necrosis factor-α -- NF-kB nuclear factor kappa -B -- COX-2 cyclooxygenase-2 -- GFAP glial fibrillary acidic protein -- iNOS inducible nitric oxide synthase -- IL-1α interleukin-1α -- IL-1β interleukin-1β -- IL-6 interleukin-6 -- P-p38 MAPK phosphorylated p38 mitogen activated protein kinase -- NO nitrite -- CNS central nervous system -- LPS lipopolysaccharide -- Th T helper cells -- NLRP3 NLR family pyrin domain containing-3 -- mTOR mammalian target of rapamycin -- Tregs T regulatory cells -- TNFR-AF3 tumor necrosis factor receptor-associated factor −3
Neurochemistry -- Periodicals
Neurochemistry -- Periodicals
Neurochimie -- Périodiques
Neurochemistry
Periodicals
612.804205 - Journal URLs:
- http://www.sciencedirect.com/science/journal/01970186 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.neuint.2018.07.003 ↗
- Languages:
- English
- ISSNs:
- 0197-0186
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 6081.317000
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- 7547.xml