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Review
. 2016;14(2):155-64.
doi: 10.2174/1570159x14666151204122017.

LPS-induced Murine Neuroinflammation Model: Main Features and Suitability for Pre-clinical Assessment of Nutraceuticals

Miryam Nava Catorce, Goar Gevorkian  1
Affiliations
Review

LPS-induced Murine Neuroinflammation Model: Main Features and Suitability for Pre-clinical Assessment of Nutraceuticals

Miryam Nava Catorce et al. Curr Neuropharmacol. 2016.

Abstract

Neuroinflammation is an important feature in the pathogenesis and progression of neurodegenerative diseases such as Alzheimer´s disease (AD), Parkinson´s disease (PD), frontotemporal dementia and amyotrophic lateral sclerosis. Based on current knowledge in the field, suggesting that targeting peripheral inflammation could be a promising additional treatment/prevention approach for neurodegenerative diseases, drugs and natural products with anti-inflammatory properties have been evaluated in animal models of neuroinflammation and neurodegeneration. In this review, we provide an extensive analysis of one of the most important and widely-used animal models of peripherally induced neuroinflammation and neurodegeneration - lipopolysaccharide (LPS)-treated mice, and address the data reproducibility in published research. We also summarize briefly basic features of various natural products, nutraceuticals, with known anti-inflammatory effects and present an overview of data on their therapeutic potential for reducing neuroinflammation in LPS-treated mice.

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References

    1. Philips T., Robberecht W. Neuroinflammation in amyotrophic lateral sclerosis: role of glial activation in motor neuron disease. Lancet Neurol. 2011;10(3):253–263. doi: 10.1016/S1474-4422(11)70015-1. - DOI - PubMed
    1. Eikelenboom P., Hoozemans J.J., Veerhuis R., van Exel E., Rozemuller A.J., van Gool W.A. Whether, when and how chronic inflammation increases the risk of developing late-onset Alzheimer’s disease. Alzheimers Res. Ther. 2012;4(3):15. doi: 10.1186/alzrt118. - DOI - PMC - PubMed
    1. Blandini F. Neural and immune mechanisms in the pathogenesis of Parkinson’s disease. J. Neuroimmune Pharmacol. 2013;8(1):189–201. doi: 10.1007/s11481-013-9435-y. - DOI - PubMed
    1. Evans M.C., Couch Y., Sibson N., Turner M.R. Inflammation and neurovascular changes in amyotrophic lateral sclerosis. Mol. Cell. Neurosci. 2013;53:34–41. - PubMed
    1. Krstic D., Knuessel I. Deciphering the mechanism underlying late-onset Alzheimer disease. Nat. Rev. Neurol. 2013;9(1):25–34. doi: 10.1038/nrneurol.2012.236. - DOI - PubMed

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