NPY leu7pro and Alcohol Dependence in Finnish and Swedish Populations

Zhu, Guoqiang; Pollak, Lotta; Mottagui‐Tabar, Salim; Wahlestedt, Claes; Taubman, Julie; Virkkunen, Matti; Goldman, David; Heilig, Markus

doi:10.1097/00000374-200301000-00004

Cited by 21 publications

(27 citation statements)

References 28 publications

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“…45 A functional polymorphism in the human NPY (Leu7Pro) resulting in increased NPY release from sympathetic nerves is associated with characteristics of metabolic syndrome and it has been suggested that the Pro7 allele is associated with an increased risk for alcohol dependence, a common comorbid disorder of ADHD. 46 In the rodent model, central administration or overexpression of NPY produces a profound increase in food intake, whereas a reduction of NPY results in a decrease (for review see Karl and Herzog 45 ). Food deprivation upregulates NPY in the arcuate nucleus of the hypothalamus, and repeated administration of NPY induces obesity.…”

Section: Discussionmentioning

confidence: 99%

Genome-wide copy number variation analysis in attention-deficit/hyperactivity disorder: association with neuropeptide Y gene dosage in an extended pedigree

et al. 2010

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Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental syndrome characterized by hyperactivity, inattention and increased impulsivity. To detect micro-deletions and micro-duplications that may have a role in the pathogenesis of ADHD, we carried out a genome-wide screen for copy number variations (CNVs) in a cohort of 99 children and adolescents with severe ADHD. Using high-resolution array comparative genomic hybridization (aCGH), a total of 17 potentially syndrome-associated CNVs were identified. The aberrations comprise 4 deletions and 13 duplications with approximate sizes ranging from 110 kb to 3 Mb. Two CNVs occurred de novo and nine were inherited from a parent with ADHD, whereas five are transmitted by an unaffected parent. Candidates include genes expressing acetylcholine-metabolizing butyrylcholinesterase (BCHE), contained in a de novo chromosome 3q26.1 deletion, and a brain-specific pleckstrin homology domaincontaining protein (PLEKHB1), with an established function in primary sensory neurons, in two siblings carrying a 11q13.4 duplication inherited from their affected mother. Other genes potentially influencing ADHD-related psychopathology and involved in aberrations inherited from affected parents are the genes for the mitochondrial NADH dehydrogenase 1 a subcomplex assembly factor 2 (NDUFAF2), the brain-specific phosphodiesterase 4D isoform 6 (PDE4D6) and the neuronal glucose transporter 3 (SLC2A3). The gene encoding neuropeptide Y (NPY) was included in a B3 Mb duplication on chromosome 7p15.2-15.3, and investigation of additional family members showed a nominally significant association of this 7p15 duplication with increased NPY plasma concentrations (empirical family-based association test, P = 0.023). Lower activation of the left ventral striatum and left posterior insula during anticipation of large rewards or losses elicited by functional magnetic resonance imaging links gene dose-dependent increases in NPY to reward and emotion processing in duplication carriers. These findings implicate CNVs of behaviour-related genes in the pathogenesis of ADHD and are consistent with the notion that both frequent and rare variants influence the development of this common multifactorial syndrome.

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Section: Discussionmentioning

confidence: 99%

Genome-wide copy number variation analysis in attention-deficit/hyperactivity disorder: association with neuropeptide Y gene dosage in an extended pedigree

et al. 2010

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“…There is also a high comorbidity of alcoholism, addiction, and cognitive dysfunction with various psychiatric conditions (3). There are several clinical studies investigating the cerebrospinal fluid (CSF) and plasma NPY concentrations in psychiatric disorders such as anxiety disorders, depression, stress related disorders, alcohol dependence, and eating disorders (18)(19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

Plasma Neuropeptide Y Levels in Medication Naive Adolescents with Major Depressive Disorder

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Öztürk³

et al. 2010

Klinik Psikofarmakoloji Bülteni-Bulletin of Clinical Psychophar

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ÖZET:‹laç tedavisi almayan majör depresif bozukluklu ergenlerde plasma nöropeptid Y düzeyleri Amaç: Neuropeptide Y (NPY), anksiyete ve depresyon patofizyolojisinde önemli bir maddedir. NPY'nin emosyonel düzenlemeyi sürdürmesi için kortikotropin sal›n›m›n› sa¤-layan faktör (CRF) taraf›ndan arac›l›k edilen stres etkilerini giderdi¤i ileri sürülmüfltür. Bu çal›flmada ilk kez depresyon tan›s› alan ergenlerde NPY düzeyleri, hastalar›n intihar giriflimi öyküleri gözününde bulundurularak araflt›r›lm›flt›r. Yöntem: Majör depresif bozukluk (MDB) tan›l› 33 ergen ça-l›flmaya al›nd›. 11 hasta, baflka bir psikiyatrik hastal›¤›n varl›¤› nedeniyle çal›flma d›fl›nda tutuldu. MDB tan›l› 22 ergende, NPY'nin plazma konsantrasyonlar› ölçüldü. Beck Depresyon Envanteri-Türkçe uyarlamas› ve Beck Anksiyete Envanteri-Türkçe uyarlamas›, depresyon ve anksiyete düzey-lerini ölçmek için kullan›ld›. Bulgular: Depresyonlu ergenlerde sa¤l›kl› kontrollere oranla anlaml› derecede düflük NPY düzeyleri bulundu. Hastalar intihar giriflimi öykülerine göre s›n›fland›r›ld›¤›nda her iki grup aras›nda NPY düzeyleri aç›s›ndan anlaml› bir fark bulunmad›. NPY düzeyleri, hastal›¤›n süresiyle ve suç-luluk duygular› ile negatif yönde, anksiyeteyle pozitif yön-de korelasyon gösterdi. Aksiyete, bir eflde¤iflken olarak al›nd›¤› zaman, NPY ile suçluluk duygular› aras›ndaki korelasyonlar kayboluyor, hastal›¤›n süresi bir eflde¤iflken olarak al›nd›¤›nda aradaki korelasyon anlaml›l›¤›n› koruyordu. Tart›flma: Ergen depresif hastalar sa¤l›kl› kontrollere oranla daha düflük NPY plazma düzeylerine sahipti. Plazma NPY düzeyleri, hastal›¤›n süresiyle azal›yor, suçluluk duygusu ve anksiyetenin fliddetiyle art›yordu. NPY'nin, ergenlerde gö-rülen MDB'de anksiyete ile ilgili depresyona bir e¤ilim için belirleyici oldu¤u ileri sürülebilir. Plasma neuropeptide Y levels in medication naive adolescents with major depressive disorder Objective: Neuropeptide Y (NPY) has been implicated in pathophysiology of anxiety and depression. It was proposed that NPY counteracts corticotropin-releasing factor-mediated stress effects to maintain emotional regulation. We investigated NPY concentrations in a sample of first episode medication-naive adolescent patients with MDD with regards to their history of suicide attempts. Method: 33 adolescents with MDD were enrolled. 11 patients were excluded due to comorbidity of another psychiatric illness. In 22 adolescents with MDD patients, the plasma concentrations of NPY were assessed. The Beck Depression Inventory-Turkish Version and the Beck Anxiety Scale-Turkish Version were used to rate the severity of depressive and anxiety symptoms. Results: Our sample of depressed patients showed lower levels of NPY compared to healthy controlsWhen the depressed patients were grouped with regards to suicidality, both groups did not show any significant differences. NPY levels were negatively correlated with duration of illness and feelings of guilt, and positively correlated with anxiety. When anxiety was taken as a covariate, significant correlations between ...

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“…Among these are monoaminergic genes involved in brain reward pathways and serotonergic genes involved in impulse control and anxiety traits (for review, see Enoch and Goldman 1 ). More recently, on the basis of animal studies, an involvement has been suggested for neuropeptide Y (NPY), 2 but human findings have been inconsistent, 3,4 possibly due to the methodological difficulties involved, and due to the limited quantitative contribution of individual loci in the complex trait of alcoholism.…”

Section: Introductionmentioning

confidence: 99%

A cluster of differentially expressed signal transduction genes identified by microarray analysis in a rat genetic model of alcoholism

et al. 2004

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Analyzing gene expression patterns in genetic models of alcoholism may uncover previously unknown susceptibility genes, and point to novel targets for drug development. Here, we compared expression profiles in alcoholpreferring AA rats with the alcohol-avoiding counterpart ANA line, and unselected Wistar rats. Cingulate cortex, Nc. accumbens, amygdala and hippocampus of each line were analyzed using the Afymetrix RN U34 arrays and dChip 1.1 software. Analysis of line-specific expression revealed 48 differentially expressed genes between AA and ANA rats. Elevated hippocampal neuropeptide Y (NPY) was found in ANA rats in agreement with previous studies. A cluster of MAP-kinases indicating altered signal transduction was upregulated within the Nc. Accumbens of the AA line, and is of particular functional interest. Within the amygdala, a more loosely inter-related cluster of cytoskeleton-associated genes may point to structural abnormalities. The observed dysregulations may contribute to the alcohol-preferring phenotype.

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NPY leu7pro and Alcohol Dependence in Finnish and Swedish Populations

Abstract: Pro7 does not seem to be associated with a diagnosis of alcoholism in Caucasian populations.

Cited by 21 publications

References 28 publications

Genome-wide copy number variation analysis in attention-deficit/hyperactivity disorder: association with neuropeptide Y gene dosage in an extended pedigree

Genome-wide copy number variation analysis in attention-deficit/hyperactivity disorder: association with neuropeptide Y gene dosage in an extended pedigree

Plasma Neuropeptide Y Levels in Medication Naive Adolescents with Major Depressive Disorder

A cluster of differentially expressed signal transduction genes identified by microarray analysis in a rat genetic model of alcoholism

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