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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.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.