{'fraction_non_alphanumeric': 0.04175222450376454, 'fraction_numerical': 0.023956194387405885, 'mean_word_length': 5.6454545454545455, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Association analysis of a PAX‐6 gene promoter‐associated polymorphic repeat with alcohol dependence

The human paired box‐containing gene PAX‐6 participates in the development and plasticity of the brain including the limbic system, the neural system that plays a crucial role in reward processes. We have reported recently a polymorphic dinucleotide repeat sequence with the structure (AC)m(AG)n, which is located ∼ 1 kb upstream of the transcription initiation site associated with promoter B and confers allelic variation of PAX‐6 expression in the human brain. In the present association study we tested whether length variation of PAX‐6 gene‐linked polymorphic region (PAX‐6 LPR) influences susceptibility to alcohol dependence.The repeat length of the PAX‐6 LPR was assessed in 354 control subjects and 328 alcohol‐dependent patients, including four subgroups with a presumed substantial genetic predisposition: (a) with a history of withdrawal complications (n=100); (b) with a history of parental alcoholism (n=115); (c) with early onset (n=67) and (d) with dissocial personality disorders (n=54). Allelic distribution of the PAX‐6 LPR did not differ significantly between the controls and the entire group of alcohol‐dependent patients (χ2=0.015, df 1, p=0.904), or any of the subgroups of patients with severe alcoholism. Our results do not provide evidence that length variation of the PAX‐6 LPR contributes to the pathogenesis of alcohol dependence.