KCNIP4 as a candidate gene for personality disorders and adult ADHD

Weissflog, L.; Scholz, Claus‐Jürgen; Jacob, Christian; Nguyen, Thuy Trang; Zamzow, Karin; Groß-Lesch, Silke; Renner, Tobias; Romanos, Marcel; Rujescu, Dan; Walitza, Susanne; Kneitz, Susanne; Lesch, Klaus‐Peter; Reif, Andreas

doi:10.1016/j.euroneuro.2012.07.017

Cited by 37 publications

(28 citation statements)

References 33 publications

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“…These are showed in Supplementary Table 1. 35, 48, 53, 54, 57, 60, 64, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113 In particular, among the most known, DRD5 , whose highly polymorphic dinucleotide repeat (CA) n has been the most studied in adults, three studies 54, 60, 80 were available, but Squassina et al 80 was excluded because no frequencies were reported. Ribases et al 48 investigated other polymorphisms.…”

Section: Resultsmentioning

confidence: 99%

“…Other genes were studied in single studies: for instance circadian locomotor output cycles kaput (CLOCK), 105 protein kinase G ( PRKG1 ), 106 mineralocorticoid receptor ( NR3C2 ), 107 CKLF-like MARVEL transmembrane domain containing 8 ( CMTM8 )/diacylglycerol kinase eta ( DGKH )/neuronal PAS domain protein 3 ( NPAS3 )/solute carrier family 39 (zinc transporter), member 3 ( SLC39A3 )/deafness, autosomal recessive 31 ( DFNB31 )/epidermal growth factor receptor ( EGFR ), 108 neural cell adhesion molecule 1 ( NCAM1 )/tetratricopeptide repeat domain 12 ( TTC12 )/ankyrin repeat and kinase domain containing 1 ( ANKK1 ), 82 Ca(2+)-binding extracellular heparan/chondroitin sulfate proteoglycan ( SPOCK3 ), 109 disrupted in schizophrenia 1 ( DISC1 ), 110 Kv channel-interacting protein 4 ( KCNIP4 ), 111 phosphatase 2, regulatory subunit B, gamma ( PPP2R2C ), 112 forkhead box P2 ( FOXP2 ), 113 αN-catenin protein (CTNNA2), 96 u-opioid receptor (OPRM1), and others. 60 Thus we did not perform meta-analyses.…”

Section: Resultsmentioning

confidence: 99%

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Attention-deficit hyperactivity disorder in adults: A systematic review and meta-analysis of genetic, pharmacogenetic and biochemical studies

2016

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The adult form of attention-deficit/hyperactivity disorder has a prevalence of up to 5% and is the most severe long-term outcome of this common disorder. Family studies in clinical samples as well as twin studies suggest a familial liability and consequently different genes were investigated in association studies. Pharmacotherapy with methylphenidate (MPH) seems to be the first-line treatment of choice in adults with attention-deficit hyperactive disorder (ADHD) and some studies were conducted on the genes influencing the response to this drug. Finally some peripheral biomarkers were identified in ADHD adult patients. We believe this work is the first systematic review and meta-analysis of candidate gene association studies, pharmacogenetic and biochemical (metabolomics) studies performed in adults with ADHD to identify potential genetic, predictive and peripheral markers linked specifically to ADHD in adults. After screening 5129 records, we selected 87 studies of which 61 were available for candidate gene association studies, 5 for pharmacogenetics and 21 for biochemical studies. Of these, 15 genetic, 2 pharmacogenetic and 6 biochemical studies were included in the meta-analyses. We obtained an association between adult ADHD and the gene BAIAP2 (brain-specific angiogenesis inhibitor 1-associated protein 2), even after Bonferroni correction, with any heterogeneity in effect size and no publication bias. If we did not apply the Bonferroni correction, a trend was found for the carriers allele 9R of dopamine transporter SLC6A3 40 bp variable tandem repeat polymorphism (VNTR) and for 6/6 homozygotes of SLC6A3 30 bp VNTR. Negative results were obtained for the 9-6 haplotype, the dopamine receptor DRD4 48 bp VNTR, and the enzyme COMT SNP rs4680. Concerning pharmacogenetic studies, no association was found for the SLC6A3 40 bp and response to MPH with only two studies selected. For the metabolomics studies, no differences between ADHD adults and controls were found for salivary cortisol, whereas lower serum docosahexaenoic acid (DHA) levels were found in ADHD adults. This last association was significant even after Bonferroni correction and in absence of heterogeneity. Other polyunsaturated fatty acids (PUFAs) such as AA (arachidonic acid), EPA (eicosapentaenoic acid) and DyLA (dihomogammalinolenic acid) levels were not different between patients and controls. No publication biases were observed for these markers. Genes linked to dopaminergic, serotoninergic and noradrenergic signaling, metabolism (DBH, TPH1, TPH2, DDC, MAOA, MAOB, BCHE and TH), neurodevelopment (BDNF and others), the SNARE system and other forty genes/proteins related to different pathways were not meta-analyzed due to insufficient data. In conclusion, we found that there were not enough genetic, pharmacogenetic and biochemical studies of ADHD in adults and that more investigations are needed. Moreover we confirmed a significant role of BAIAP2 and DHA in the etiology of ADHD exclusively in adults. Future research should be focused on the replication ...

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Attention-deficit hyperactivity disorder in adults: A systematic review and meta-analysis of genetic, pharmacogenetic and biochemical studies

2016

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“…In addition, CSMD1 , the gene with FWH signatures in the most lineages ( Homo sapiens, Pan paniscus, Pan troglodytes ellioti, Pan troglodytes schweinfurthii, Gorilla gorilla gorilla and Pongo pygmaeus ) (supplementary table S73, Supplementary Material online), whose function is unknown but that is highly expressed in the central nervous system (Kraus et al 2006) and harbors variants associated with schizophrenia (Håvik et al 2011). Further, of the four genes with FWH signatures in five lineages, two are associated with neuronal phenotypes: KCNIP4 , which encodes an A-type potassium channel modulatory protein, and harbors variants associated with attention deficit hyperactive disorder (Weißflog et al 2013) and NRG3 (Neuregulin 3), which is crucial in the development of the nervous system and whose variants are associated to schizophrenia (Chen et al 2009). …”

Section: Discussionmentioning

confidence: 99%

Natural Selection in the Great Apes

et al. 2016

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Natural selection is crucial for the adaptation of populations to their environments. Here, we present the first global study of natural selection in the Hominidae (humans and great apes) based on genome-wide information from population samples representing all extant species (including most subspecies). Combining several neutrality tests we create a multi-species map of signatures of natural selection covering all major types of natural selection. We find that the estimated efficiency of both purifying and positive selection varies between species and is significantly correlated with their long-term effective population size. Thus, even the modest differences in population size among the closely related Hominidae lineages have resulted in differences in their ability to remove deleterious alleles and to adapt to changing environments. Most signatures of balancing and positive selection are species-specific, with signatures of balancing selection more often being shared among species. We also identify loci with evidence of positive selection across several lineages. Notably, we detect signatures of positive selection in several genes related to brain function, anatomy, diet and immune processes. Our results contribute to a better understanding of human evolution by putting the evidence of natural selection in humans within its larger evolutionary context. The global map of natural selection in our closest living relatives is available as an interactive browser at http://tinyurl.com/nf8qmzh.

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“…In this context, the use of high density SNP panels has allowed the identification of genetic markers associated with phenotypes of interest (Settles and others 2009, Wilson and others 2012). Evidence of a genetic predisposition to PFTS has been recently presented (Ramis and others 2015).…”

Section: Discussionmentioning

confidence: 99%

Genome‐wide association study of periweaning failure‐to‐thrive syndrome (PFTS) in pigs

Zanella

Morés

et al. 2016

Veterinary Record

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Porcine periweaning-failure-to-thrive syndrome (PFTS) is a condition that affects newly weaned piglets. It is characterised by a progressive debilitation leading to death, in the absence of infectious, nutritional, management or environmental factors. In this study, we present the first report of PFTS in South America and the results of a genome-wide association study to identify the genetic markers associated with the appearance of this condition in a crossbred swine population. Four chromosomal regions were associated with PFTS predisposition, one located on SSCX, one on SSC8, and the two other regions on SSC14. Regions on SSC8 and SSC14 harbour important functional candidate genes involved in human depression and might have an important role in PFTS. Our findings contribute to the increasing knowledge about this syndrome, which has been investigated since 2007, and to the identification of the aetiology of this disease.

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KCNIP4 as a candidate gene for personality disorders and adult ADHD

Cited by 37 publications

References 33 publications

Attention-deficit hyperactivity disorder in adults: A systematic review and meta-analysis of genetic, pharmacogenetic and biochemical studies

Attention-deficit hyperactivity disorder in adults: A systematic review and meta-analysis of genetic, pharmacogenetic and biochemical studies

Natural Selection in the Great Apes

Genome‐wide association study of periweaning failure‐to‐thrive syndrome (PFTS) in pigs

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