Dataset Information

Medications Development for the Treatment of Nicotine Dependence in Individuals with Schizophrenia.

ABSTRACT: The development of medications for the treatment of nicotine dependence in patients with schizophrenia is a public health priority due to its high prevalence rates, devastating medical consequences, and difficulty to treat. It has been hypothesized that the high prevalence of nicotine dependence among patients with schizophrenia may be due to a shared neurobiological vulnerability. This shared vulnerability has been evidenced in reports showing that nicotine improves neuropsychological deficits associated with schizophrenia such as in the P50 evoked auditory potentials, spatial working memory, and attention. The common pathophysiologic pathways of smoking and schizophrenia may serve as the basis for the pharmacological evaluation of medications for the treatment of these concurrent disorders. Currently, little research of medications for the treatment of this comorbidity has been conducted. Studies have evaluated the efficacy of smoking cessation medications in patients with schizophrenia. These include the nicotine replacement therapy (patch, nasal spray) and sustained release bupropion. Others have evaluated the anti-smoking effect of medications (e.g., clozapine, haloperidol) used for the treatment of schizophrenia. In both cases, the results have not been conclusive. Newer smoking cessation approaches such as varenicline, selegiline, rimonabant, and nicotine vaccine, among others, have yet to be tested in this population. The purpose of this article is to review the results of the studies conducted to date and propose some potential pharmacotherapies based on the current knowledge of the pathophysiology of both disorders.

SUBMITTER: Montoya ID

PROVIDER: S-EPMC2633934 | biostudies-literature | 2007 Nov

REPOSITORIES: biostudies-literature

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Medications Development for the Treatment of Nicotine Dependence in Individuals with Schizophrenia.

Montoya Ivan D ID Vocci Frank F

Journal of dual diagnosis 20071101 3-4

The development of medications for the treatment of nicotine dependence in patients with schizophrenia is a public health priority due to its high prevalence rates, devastating medical consequences, and difficulty to treat. It has been hypothesized that the high prevalence of nicotine dependence among patients with schizophrenia may be due to a shared neurobiological vulnerability. This shared vulnerability has been evidenced in reports showing that nicotine improves neuropsychological deficits ...[more]

PMID: 19194522

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Project description:IntroductionHeritability estimates of nicotine dependence (ND) range from 40% to 70%, but discovery GWAS of ND are underpowered and have limited predictive utility. In this work, we leverage genetically correlated traits and diseases to increase the accuracy of polygenic risk prediction.MethodsWe employed a multi-trait model using summary statistic-based best linear unbiased predictors (SBLUP) of genetic correlates of DSM-IV diagnosis of ND in 6394 individuals of European Ancestry (prevalence = 45.3%, %female = 46.8%, µ age = 40.08 [s.d. = 10.43]) and 3061 individuals from a nationally-representative sample with Fagerström Test for Nicotine Dependence symptom count (FTND; 51.32% female, mean age = 28.9 [s.d. = 1.70]). Polygenic predictors were derived from GWASs known to be phenotypically and genetically correlated with ND (i.e., Cigarettes per Day [CPD], the Alcohol Use Disorders Identification Test [AUDIT-Consumption and AUDIT-Problems], Neuroticism, Depression, Schizophrenia, Educational Attainment, Body Mass Index [BMI], and Self-Perceived Risk-Taking); including Height as a negative control. Analyses controlled for age, gender, study site, and the first 10 ancestral principal components.ResultsThe multi-trait model accounted for 3.6% of the total trait variance in DSM-IV ND. Educational Attainment (β = -0.125; 95% CI: [-0.149,-0.101]), CPD (0.071 [0.047,0.095]), and Self-Perceived Risk-Taking (0.051 [0.026,0.075]) were the most robust predictors. PGS effects on FTND were limited.ConclusionsRisk for ND is not only polygenic, but also pleiotropic. Polygenic effects on ND that are accessible by these traits are limited in size and act additively to explain risk.ImplicationsThese findings enhance our understanding of inherited genetic factors for nicotine dependence. The data show that genome-wide association study (GWAS) findings across pre- and comorbid conditions of smoking are differentially associated with nicotine dependence and that when combined explain significantly more trait variance. These findings underscore the utility of multivariate approaches to understand the validity of polygenic scores for nicotine dependence, especially as the power of GWAS of broadly-defined smoking behaviors increases. Realizing the potential of GWAS to inform complex smoking behaviors will require similar theory-driven models that reflect the myriad of mechanisms that drive individual differences.

Dataset Information

Medications Development for the Treatment of Nicotine Dependence in Individuals with Schizophrenia.

Publications

Medications Development for the Treatment of Nicotine Dependence in Individuals with Schizophrenia.

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