Nicotine therapeutic benefits: Difference between revisions
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Multiple Sclerosis |
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==Movement Disorders (not diagnosis specific)== | ==Movement Disorders (not diagnosis specific)== | ||
==Multiple Sclerosis - Humans / Experimental Autoimmune Encephalomyelitis (EAE) - Animals== | ==Multiple Sclerosis - Humans / Experimental Autoimmune Encephalomyelitis (EAE) - Animals== | ||
===2016 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760232/ Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis]=== | |||
*Animal Study | |||
* This study provides evidence that nicotine alters the infiltration of proinflammatory monocytes and neutrophils into the CNS of [[Abbreviations|EAE]] mice via multiple [[Abbreviations|nAChRs]], including the α7 and α9 subtypes. Nicotine appears to achieve these effects by inhibiting the expression of CCL2 and CXCL2, two cytokines involved in the chemotaxis of proinflammatory monocytes and neutrophils, respectively. The use of ligands that are selective for one or both of these nAChR subtypes may offer a beneficial clinical outcome, and thus provide a valuable therapeutic strategy for neuroinflammatory disorders such as MS. | |||
*[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760232/pdf/1501613.pdf PDF Version] | |||
*Citation: Jiang W, St-Pierre S, Roy P, Morley BJ, Hao J, Simard AR. Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis. J Immunol. 2016 Mar 1;196(5):2095-108. doi: 10.4049/jimmunol.1501613. Epub 2016 Jan 25. PMID: 26810225; PMCID: PMC4760232. | |||
*Acknowledgements: This work was supported by grants from the Multiple Sclerosis Society of Canada (to A.R.S.), the New Brunswick Health Research Foundation (to A.R.S.), the New Brunswick Innovation Foundation (to A.R.S.), the Nebraska Tobacco Settlement Biomedical Research Fund (to B.J.M.), and the National Institutes of Health (Grant R01DC006907 to B.J.M.). Salary support was provided by the Centre de Formation Médicale du Nouveau-Brunswick (to W.J.) and the New Brunswick Innovation Foundation (to S.S-P. and P.R.). | |||
*See Also - Related article: [https://mssociety.ca/research-news/article/ms-society-funded-study-shows-that-nicotine-reduces-the-invasion-of-harmful-immune-cells-into-the-brain-in-mice-with-an-ms-like-disease MS Society-funded study shows that nicotine reduces the invasion of harmful immune cells into the brain in mice with an MS-like disease] | |||
===2014 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176721/ The Experimental Autoimmune Encephalomyelitis Disease Course Is Modulated by Nicotine and Other Cigarette Smoke Components]=== | |||
*Animal Study | |||
*Our results show that nicotine reduces the severity of EAE, as shown by reduced demyelination, increased body weight, and attenuated microglial activation. Nicotine administration after the development of EAE symptoms prevented further disease exacerbation, suggesting that it might be useful as an [[Abbreviations|EAE/MS]] therapeutic. In contrast, the remaining components of cigarette smoke, delivered as cigarette smoke condensate (CSC), accelerated and increased adverse clinical symptoms during the early stages of EAE. | |||
*[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176721/pdf/pone.0107979.pdf PDF Version] | |||
*Citation: Gao Z, Nissen JC, Ji K, Tsirka SE. The experimental autoimmune encephalomyelitis disease course is modulated by nicotine and other cigarette smoke components. PLoS One. 2014 Sep 24;9(9):e107979. doi: 10.1371/journal.pone.0107979. PMID: 25250777; PMCID: PMC4176721. | |||
*Acknowledgements: This work was supported by National Multiple Sclerosis Society awards CA1044A1 and PP181, National Aeronautics and Space Administration NNA14AB04A and National Institutes of Health R01NS42168 (ST), and National Institutes of Health K12GM102778 to JN. | |||
===2013 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659034/ Novel Therapeutic Approach by Nicotine in Experimental Model of Multiple Sclerosis]=== | |||
*Animal Study | |||
*Due to the proven therapeutic effect of nicotine on AD (Alzheimer’s Disease) and PD (Parkinson’s Disease), we decided to study the role of nicotine in [[Abbreviations|EAE]] as an animal model of MS. Our treatment group showed less inflammation in histopathological evaluation along with myelin sheet protection. Moreover, prevention group showed less inflammation compared with treatment group. Thus, nicotine might be recommended as a promising drug for [[Abbreviations|MS]] therapy. | |||
*[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659034/pdf/icns_10_4_20.pdf PDF Version] | |||
*Citation: Naddafi F, Reza Haidari M, Azizi G, Sedaghat R, Mirshafiey A. Novel therapeutic approach by nicotine in experimental model of multiple sclerosis. Innov Clin Neurosci. 2013 Apr;10(4):20-5. PMID: 23696955; PMCID: PMC3659034. | |||
==OCD (Obsessive Compulsive Disorder)== | ==OCD (Obsessive Compulsive Disorder)== | ||