Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2008-4-18
pubmed:abstractText
Eating disorders (EDs) are complex psychiatric diseases that include anorexia nervosa and bulimia nervosa, and have higher than 50% heritability. Previous studies have found association of BDNF and NTRK2 to ED, while animal models suggest that other neurotrophin genes might also be involved in eating behavior. We have performed a family-based association study with 151 TagSNPs covering 10 neurotrophin signaling genes: NGFB, BDNF, NTRK1, NGFR/p75, NTF4/5, NTRK2, NTF3, NTRK3, CNTF and CNTFR in 371 ED trios of Spanish, French and German origin. Besides several nominal associations, we found a strong significant association after correcting for multiple testing (P = 1.04 x 10(-4)) between ED and rs7180942, located in the NTRK3 gene, which followed an overdominant model of inheritance. Interestingly, HapMap unrelated individuals carrying the rs7180942 risk genotypes for ED showed higher levels of expression of NTRK3 in lymphoblastoid cell lines. Furthermore, higher expression of the orthologous murine Ntrk3 gene was also detected in the hypothalamus of the anx/anx mouse model of anorexia. Finally, variants in NGFB gene appear to modify the risk conferred by the NTRK3 rs7180942 risk genotypes (P = 4.0 x 10(-5)) showing a synergistic epistatic interaction. The reported data, in addition to the previous reported findings for BDNF and NTRK2, point neurotrophin signaling genes as key regulators of eating behavior and their altered cross-regulation as susceptibility factors for EDs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1460-2083
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1234-44
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:18203754-Adolescent, pubmed-meshheading:18203754-Adult, pubmed-meshheading:18203754-Animals, pubmed-meshheading:18203754-Cell Line, Tumor, pubmed-meshheading:18203754-Computational Biology, pubmed-meshheading:18203754-Disease Models, Animal, pubmed-meshheading:18203754-Eating Disorders, pubmed-meshheading:18203754-Family, pubmed-meshheading:18203754-Female, pubmed-meshheading:18203754-France, pubmed-meshheading:18203754-Gene Expression Regulation, pubmed-meshheading:18203754-Germany, pubmed-meshheading:18203754-Haplotypes, pubmed-meshheading:18203754-Humans, pubmed-meshheading:18203754-Mice, pubmed-meshheading:18203754-Nerve Growth Factor, pubmed-meshheading:18203754-Nerve Growth Factors, pubmed-meshheading:18203754-Polymorphism, Single Nucleotide, pubmed-meshheading:18203754-Receptor, trkC, pubmed-meshheading:18203754-Signal Transduction, pubmed-meshheading:18203754-Spain
pubmed:year
2008
pubmed:articleTitle
Association of NTRK3 and its interaction with NGF suggest an altered cross-regulation of the neurotrophin signaling pathway in eating disorders.
pubmed:affiliation
Genes and Disease Program, Center for Genomic Regulation, 08003 Barcelona, Catalonia, Spain.
pubmed:publicationType
Journal Article, Clinical Trial, Research Support, Non-U.S. Gov't