Nicotine therapeutic benefits: Difference between revisions

* 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.

*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.

*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.

*Nicotine may ameliorate OC symptoms in severe, treatment-refractory [[Abbreviations|OCD]] patients. Although encouraging, these initial positive effects should be tested in large controlled studies.

*Intraperitoneal nicotine administration controls neuropathic pain evoked by traumatic or toxic nervous system alterations. These results support the nAChR modulation as a possible therapeutic approach to the complex, undertreated chemotherapy-induced neuropathies.  

*The preoperative application of a 7 mg nicotine patch resulted in a significant reduction in postoperative opioid consumption in nonsmoking men undergoing [[Abbreviations|RRP]] in this study. Its use was generally well tolerated, but the maximum nausea scores were higher in patients who received nicotine.

*At 26 year follow-up, women with greater dietary nicotine intake had a lower risk of [[Abbreviations|Parkinson Disease (PD)]] than those with lower intake. Dietary nicotine intake was calculated based on consumption of peppers, tomatoes, processed tomatoes, potatoes, and tea.  

*Acknowledgements: Supported by National Institute of Neurological Disorders and Stroke at the NIH grant 1R03NS093245-01A1 (to XG). The Nurses’ Health Study

is supported by the NIH through grant UM1 CA186107. The Health Professionals Follow-up Study cohort is supported by the NIH through grant U01 CA167552.

*Nicotine may have therapeutic uses in the treatment of [[Abbreviations|Parkinson's Disease]].

*When chronically taken, nicotine may result in: protection against Parkinson's Disease (other diseases mentioned in study)

*The immune phenotype of patients with symptomatic [[wikipedia:Sarcoidosis|sarcoidosis]] treated with nicotine closely resembled that of asymptomatic patients, supporting the notion that nicotine treatment may be beneficial in this patient population.

*In this individual with refractory [[Abbreviations|ADNFLE]], nicotine had a therapeutic effect on seizures, and it may be useful to others with this disorder.

*Primary impact to the spinal cord results in stimulation of secondary processes that potentiate the initial trauma. Recent evidence indicates that nicotine can exert potent antioxidant and neuroprotective effects in [[Abbreviations|spinal cord injury (SCI)]].

*The results of the present study indicate that [[Abbreviations|iNOS]] is induced in the early stages of SCI, leading to increased nitration of protein tyrosine residues and potentiation of inflammatory responses. Microglial cells appear to be the main cellular source of iNOS in SCI. In addition, nicotine-induced anti-inflammatory effects in SCI are mediated, at least in part, by the attenuation of iNOS overexpression through the receptor-mediated mechanism. This data may have significant therapeutic implications for the targeting of nicotine receptors in the treatment of compressive spinal cord trauma.

*[[Abbreviations|Transdermal nicotine (TNP)]] was superior to placebo in reducing behavioral symptoms when patients were receiving an optimal dose of haloperidol, when the dose of haloperidol was reduced by 50%, and when the patch had been discontinued for 2 weeks. These findings confirm earlier open-label findings and suggest that combining nicotinic receptor modulation and neuroleptics could be a therapeutic option for the treatment of Tourette's disorder.

*Within 24 hr of the application of a single 7-mg [[Abbreviations|TNP (nicotine patch)]], the severity and frequency of tic symptoms is significantly decreased over baseline. This response is rapid, often reaching its maximum in the first 3 hr after application of a single patch. The duration of therapeutic effect of a single 7-mg TNP is variable and may last for about l-2 weeks.

*Application of a 7-mg TNP to children and adolescents with [[Abbreviations|TS]] appears to be clinically safe, with transient side effects. However, no child under 8 years of age and weighing less than 25 kg was considered for TNP treatment.

*nicotine may have therapeutic uses in the treatment of [[Abbreviations|Gilles de la Tourette’s syndrome (TS)]].

* Sixteen Tourette's syndrome patients, aged 9 to 15 years, whose symptoms were not controlled with neuroleptics, were followed for various lengths of time after the application of one 7 mg [[Abbreviations|transdermal nicotine patch (TNP)]] for 24 hours. While there was a broad range in individual response, application of the TNP produced significant reductions in [[Abbreviations|Yale Global Tic Severity Scale (YGTSS)]] scores relative to baseline, with an average duration of effect lasting between 1 and 2 weeks. Side effects, for the most part, were transient.

*In this study, nicotine markedly potentiated haloperidol effects in treating [[Abbreviations|TD]], and showed lesser effects on TD when used alone.