NPY leu7pro and Alcohol Dependence in Finnish and Swedish Populations (original) (raw)
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Alcoholism-clinical and Experimental Research, 2005
Background: Neuropeptide Y (NPY) is a major endogenous regulator of anxiety-related behaviors and emotionality. Transgenic work with NPY and null-mutant mice have implicated NPY in the control of alcohol consumption, suggesting that genetic variation of the prepro-NPY gene may also contribute to the heritability of alcoholism. The aim of this study was to examine whether polymorphic variants of the NPY gene are associated with the diagnosis of alcohol dependence.
Association of Neuropeptide Y Polymorphism With the Occurrence of Type 1 and Type 2 Alcoholism
Alcoholism: Clinical and Experimental Research, 2001
The susceptibility to alcoholism can be explained partially by genetic factors. Neuropeptide Y (NPY) has emerged as one potential factor contributing the development of alcoholism. A recent study indicated that the NPY gene variant producing a leucine-to-proline substitution (T to C at position 1128) was associated with 34% higher average alcohol consumption.
KLINIK PSIKOFARMAKOLOJI BULTENI-BULLETIN OF CLINICAL PSYCHOPHARMACOLOGY, 2015
Objective: Alcoholism is associated with genetic variants of genes related to alcohol metabolizing enzymes, dopaminergic, gamma-aminobutyric acidergic, glutamatergic, opioid, cholinergic, and serotonergic systems. Neurpeptide Y system and Neurexins were shown to be associated with alcohol dependence. Recent studies identified new genetic polymorphisms related to endogenous cannabinoid system, neuropetide Y and neurexin. In the present study, we aimed to investigate the association of Neurpeptide Y LEU7PRO rs16139 and neurexin 3 gene rs760288 polymorphisms with alcohol dependence in patients with alcohol dependence and healthy control subjects. Methods: 123 patients who were diagnosed with alcohol dependence according to the DSM-IV criteria and 159 healthy volunteers were included in the study. Blood samples were used to investigate polymorphisms. The genotyping of the neurexin 3 gene rs760288 and the neuropetide Y gene Leu7Pro rs16139 polymorphisms was performed using TaqMan SNP Genotyping Assays Real-Time PCR System. Results: Of the 2 genetic polymorphisms investigated in the present study, we detected association between and neurexin 3 gene rs760288 polymorphisms with alcohol dependence. Conclusions: Neurexin gene polymorphisms might be an important factor in development of alcohol addiction.
Neuropeptide Y and Alcoholism: Genetic, Molecular, and Pharmacological Evidence
Alcoholism: Clinical & Experimental Research, 2003
This article presents the proceedings of a symposium presented at the combined meeting of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism, held in San Francisco, CA, in June 2002. The organizers and chairpersons were Subhash C. Pandey and Todd E. Thiele. The presentations were (1) Altered ethanol-induced sedation and ethanol drinking in mutant mice lacking specific NPY receptor, by Todd E. Thiele; (2) NPY in P and NP rats: polymorphism and mRNA expression, by Lucinda G. Carr; (3) The cAMP-dependent PKA in the central amygdala regulates alcohol intake through NPY gene, by Subhash C. Pandey; (4) Involvement of NPY in alcohol dependence: from animal models to human genetics, by Markus Heilig; and (5) Association of neuropeptide Y polymorphism with the occurrence of type 1 and type 2 alcoholism, by Erkki Ilveskoski.
Neuroscience, 2005
Using animal models of alcoholism, previous studies suggest that neuropeptide Y (NPY) may be implicated in alcohol preference and consumption due to its role in the modulation of feeding and anxiety. Quantitative trait loci (QTL) analysis previously identified an interval on rat chromosome 4 that is highly associated with alcohol preference and consumption using an F2 population derived from inbred alcohol-preferring (iP) and-nonpreferring (iNP) rats. NPY mapped to the peak of this QTL region and was prioritized as a candidate gene for alcohol-seeking behavior in the iP and iNP rats. In order to identify a potential mechanism for reduced NPY protein levels documented in the iP rat, genetic and molecular components that influence NPY expression were analyzed between iP and iNP rats. Comparing the iP rat to the iNP rat, quantitative real-time polymerase chain reaction detected significantly decreased levels of NPY mRNA expression in the iP rat in the six brain regions tested: nucleus accumbens, frontal cortex, amygdala, hippocampus, caudate-putamen, and hypothalamus. In addition, the functional significance of three previously identified polymorphisms was assessed using in vitro expression analysis. The polymorphism defined by microsatellite marker D4Mit7 in iP rats reduced luciferase reporter gene expression in SK-N-SH neuroblastoma cells. These results suggest that differential expression of the NPY gene resulting from the D4mit7 marker polymorphism may contribute to reduced levels of NPY in discrete brain regions in the iP rats.
Addiction Biology, 2014
The functional polymorphism Asn 107 Ile (rs324981, A > T) of the neuropeptide S receptor (NPSR1) gene is involved in the modulation of traits that affect alcohol use. Hence, we have examined whether the NPSR1 A/T polymorphism is associated with alcohol use disorders (AUD) and alcohol use in a population-representative sample. Lifetime AUD were assessed by the MINI psychiatric interview (n = 501) in the older cohort of the longitudinal Estonian Children Personality Behaviour and Health Study at age 25. Alcohol use, environmental adversities and personality were reported by both the younger (original n = 583) and the older cohort (original n = 593) in three study waves. NPSR1 associations with AUD and alcohol use differed by sex. In females, both AUD [odds ratio (OR) = 7.20 (0.94-55.0), P = 0.029] and harmful alcohol use were more prevalent in A-allele carriers. In contrast, in males, AUD was more frequent in T-allele carriers [OR = 2.75 (1.19-6.36), P = 0.017], especially if exposed to adverse environments at age 15 [OR = 10 (1.18-84.51), P = 0.019]. Alcohol use was higher in male T-allele carriers at ages 15 and 18 as well. Similarly to females, however, the risk allele for higher alcohol use for males at age 25 was the A-allele. Many of the effects on alcohol use were explained by genotype effects on measures of personality. In the general population, the NPSR1 Asn 107 Ile polymorphism is associated with AUD and alcohol consumption, dependent on sex, environment and age. The results are in line with the impulsivity and personality regulating role of the NPSR1.