ArticleEuropean archives of psychiatry and clinical neuroscience2015
Genetic variation in the G72 gene is associated with increased frontotemporal fiber tract integrity.
Article in European archives of psychiatry and clinical neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Effect of DAOA genetic variation on white matter alteration in corpus callosum in patients with first-episode schizophrenia.Brain imaging and behavior · 2021Article
- G72 primate-specific gene: a still enigmatic element in psychiatric disorders.Cellular and molecular life sciences : CMLS · 2016Review
- Classification and neurobiological concepts of mania, bipolar disorder and major depression.European archives of psychiatry and clinical neuroscience · 2015Article
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15 authors.
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Abstract
G72 (syn. DAOA, D-amino acid oxidase activator) is a susceptibility gene for both schizophrenia and bipolar disorder. Diffusion tensor imaging studies hint at changes in fiber tract integrity in both disorders. We aimed to investigate whether a G72 susceptibility haplotype causes changes in fiber tract integrity in young healthy subjects. We compared fractional anisotropy in 47 subjects that were either homozygous for the M23/M24 risk haplotype (n = 20) or homozygous for M23(rs3918342)/M24(rs1421292) wild type (n = 27) using diffusion tensor imaging with 3 T. Tract-based spatial statistics, a method especially developed for diffusion data analysis, was used to delineate the major fiber tracts. We found clusters of increased FA values in homozygous risk haplotype carriers in the right periinsular region and in the right inferior parietal lobe (IPL). We did not find clusters indicating decreased FA values. The insula and the IPL have been implicated in both schizophrenia and bipolar pathophysiology. Increased FA values might reflect changes in dendritic morphology as previously described by in vitro studies. These findings further corroborate the hypothesis that a shared gene pool between schizophrenia and bipolar disorder might lead to neuroanatomic changes that confer an unspecific vulnerability for both disorders.
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