Naslov
An association between the PPARα-L162V polymorphism and nicotine dependency among patients with schizophreniaand nicotine dependency among patients with schizophrenia
(An association between the PPARα-L162V polymorphism and nicotine dependency among patients with schizophreniaand nicotine dependency among patients with schizophrenia)

Autori
Nadalin, Sergej ; Buretić-Tomljanović, Alena ; Rebić, Jelena ; Pleša, Ivana ; Šendula Jengić, Vesna

Izvornik
Comprehensive psychiatry (0010-440X) 70 (2016); 118-124

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
activated receptor-alpha ; plasma-lipid concentrations ; PPARα ; tobacco smoking ; cigarette-smoking ; antipsychotic-drugs ; monoamine-oxidase ; dopamine neurons ; L162V mutation ; in-vitro

Sažetak
Objective: Patients with schizophrenia are more likely to be smokers than the general population, which makes them an interesting group with which to study the etiology of nicotine dependency. We studied the prevalence of a gene variant of peroxisome proliferator-activated receptor alpha (PPAR alpha) in schizophrenia, together with nicotine dependency, to investigate whether the PPAR alpha-L162V polymorphism (rs1800206) influences nicotine dependency in schizophrenia. Given evidence suggesting that smoking influences the severity of schizophrenia, together with our recent data linking the PPAR alpha-L162V polymorphism to clinical manifestations of schizophrenia (in the Croatian population), we hypothesized that interactions between the two (smoking and the PPAR alpha-L162V polymorphism) might contribute to disease onset and scores for the Positive and Negative Syndrome Scale. To the best of our knowledge, this is the first study to investigate the possible associations between the PPAR alpha gene and nicotine dependency. Patients and methods: Genotyping was performed for 267 chronically ill schizophrenia patients (males/females: 140/127) by polymerase chain reaction. Results: A significant excess of PPAR alpha-L162V genotypes and PPAR alpha-162V alleles were detected among female smokers in comparison to female nonsmokers (18.2% vs. 2.0%, and 9.1% vs. 1.0%, p < 0.01, respectively). We also revealed a significant PPAR alpha genotype smoking interaction that predicted positive symptom severity among male patients (F = 4.43, p < 0.05). These data indicated that the PPAR alpha-L162V heterozygous genotype, depending on smoking status, might be of relevance as either protective, or a risk factor, for the severity of positive symptoms. No interaction between the PPAR alpha-L162V polymorphism and smoking for the time of onset of schizophrenia was detected (p > 0.05, respectively). Conclusion: We demonstrated two significant yet weak effects. The first showed an effect of the PPAR alpha-L162V polymorphism on the risk of nicotine dependency. The second linked the PPAR alpha genotype smoking interaction to positive symptoms severity among schizophrenia patients ; both effects manifested in a gender-specific fashion.

Izvorni jezik
Engleski

Znanstvena područja
Kliničke medicinske znanosti

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