Simon McCarthy-Jones1, Melissa J Green2, Rodney J Scott3, Paul A Tooney4, Murray J Cairns4, Jing Qin Wu4, Christopher Oldmeadow5, Vaughan Carr6. 1. ARC Centre of Excellence in Cognition and its Disorders, Department of Cognitive Science, Macquarie University, NSW, Australia. Electronic address: s.mccarthyjones@gmail.com. 2. ARC Centre of Excellence in Cognition and its Disorders, Department of Cognitive Science, Macquarie University, NSW, Australia; School of Psychiatry, Faculty of Medicine, University of New South Wales, NSW, Australia; Schizophrenia Research Institute, Sydney, NSW, Australia. 3. Schizophrenia Research Institute, Sydney, NSW, Australia; School of Biomedical Sciences and Pharmacy, Faculty of Health, The University of Newcastle, Callaghan, NSW 2308, Australia; Centre for Brain and Mental Health and Centre for Information-Based Medicine, University of Newcastle, Newcastle, NSW, Australia; Hunter Medical Research Institute, NSW, Australia; Hunter Area Pathology Service, Newcastle, NSW, Australia. 4. Schizophrenia Research Institute, Sydney, NSW, Australia; School of Biomedical Sciences and Pharmacy, Faculty of Health, The University of Newcastle, Callaghan, NSW 2308, Australia; Centre for Brain and Mental Health and Centre for Information-Based Medicine, University of Newcastle, Newcastle, NSW, Australia; Hunter Medical Research Institute, NSW, Australia. 5. Hunter Medical Research Institute, NSW, Australia; Faculty of Health, University of Newcastle, NSW, Australia. 6. School of Psychiatry, Faculty of Medicine, University of New South Wales, NSW, Australia; Schizophrenia Research Institute, Sydney, NSW, Australia.
Abstract
OBJECTIVE: The FOXP2 gene is involved in the development of speech and language. As some single nucleotide polymorphisms (SNPs) of FOXP2 have been found to be associated with auditory verbal hallucinations (AVHs) at trend levels, this study set out to undertake the first examination into whether interactions between candidate FOXP2 SNPs and environmental factors (specifically, child abuse) predict the likelihood of AVHs. METHOD: Data on parental child abuse and FOXP2 SNPs previously linked to AVHs (rs1456031, rs2396753, rs2253478) were obtained from the Australian Schizophrenia Research Bank for people with schizophrenia-spectrum disorders, both with (n = 211) and without (n = 122) a lifetime history of AVHs. RESULTS: Genotypic frequencies did not differ between the two groups; however, logistic regression found that childhood parental emotional abuse (CPEA) interacted with rs1456031 to predict lifetime experience of AVH. CPEA was only associated with significantly higher levels of AVHs in people with CC genotypes (odds ratio = 4.25), yet in the absence of CPEA, people with TT genotypes had significantly higher levels of AVHs than people with CC genotypes (odds ratio = 4.90). This interaction was specific to auditory verbal hallucinations, and did not predict the likelihood of non-verbal auditory hallucinations. CONCLUSIONS: Our findings offer tentative evidence that FOXP2 may be a susceptibility gene for AVHs, influencing the probability people experience AVHs in the presence and absence of CPEA. However, these findings are in need of replication in a larger study that addresses the methodological limitations of the present investigation.
OBJECTIVE: The FOXP2 gene is involved in the development of speech and language. As some single nucleotide polymorphisms (SNPs) of FOXP2 have been found to be associated with auditory verbal hallucinations (AVHs) at trend levels, this study set out to undertake the first examination into whether interactions between candidate FOXP2 SNPs and environmental factors (specifically, child abuse) predict the likelihood of AVHs. METHOD: Data on parental child abuse and FOXP2 SNPs previously linked to AVHs (rs1456031, rs2396753, rs2253478) were obtained from the Australian Schizophrenia Research Bank for people with schizophrenia-spectrum disorders, both with (n = 211) and without (n = 122) a lifetime history of AVHs. RESULTS: Genotypic frequencies did not differ between the two groups; however, logistic regression found that childhood parental emotional abuse (CPEA) interacted with rs1456031 to predict lifetime experience of AVH. CPEA was only associated with significantly higher levels of AVHs in people with CC genotypes (odds ratio = 4.25), yet in the absence of CPEA, people with TT genotypes had significantly higher levels of AVHs than people with CC genotypes (odds ratio = 4.90). This interaction was specific to auditory verbal hallucinations, and did not predict the likelihood of non-verbal auditory hallucinations. CONCLUSIONS: Our findings offer tentative evidence that FOXP2 may be a susceptibility gene for AVHs, influencing the probability people experience AVHs in the presence and absence of CPEA. However, these findings are in need of replication in a larger study that addresses the methodological limitations of the present investigation.
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