Effects of the BDNF val66met polymorphism on prefrontal brain function in a population at high genetic risk of schizophrenia
| Autor: | Eve C. Johnstone, Stephen M. Lawrie, Heather C. Whalley, David G. Cunningham-Owens, Benjamin J. Baig, Jeremy Hall, Dominic Job, Andrew M. McIntosh |
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| Rok vydání: | 2009 |
| Předmět: |
Adult
Male Risk Psychosis Adolescent Genotype Population Prefrontal Cortex Single-nucleotide polymorphism Neuropsychological Tests Bioinformatics Brain mapping Gyrus Cinguli Polymorphism Single Nucleotide Cellular and Molecular Neuroscience Young Adult medicine Humans Genetic Predisposition to Disease education Genetics (clinical) Default mode network Anterior cingulate cortex Brain-derived neurotrophic factor education.field_of_study Brain Mapping business.industry Brain-Derived Neurotrophic Factor Brain morphometry medicine.disease Magnetic Resonance Imaging Psychiatry and Mental health medicine.anatomical_structure Amino Acid Substitution Schizophrenia Female business |
| Zdroj: | American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics. (8) |
| ISSN: | 1552-485X |
| Popis: | A single nucleotide polymorphism (val66met) in the brain derived neurotrophic factor (BDNF) gene has been shown to be a risk factor for a number of psychiatric disorders, including schizophrenia. This polymorphism has also been shown to have effects on prefrontal brain morphology and function. This study aims to clarify the effects of the val66met polymorphism on prefrontal brain function in a population at high genetic risk for schizophrenia. The Edinburgh High Risk Study has followed young individuals who had one first- or second-degree relative with schizophrenia and a minimum of one further genetic relative with the illness. A sample of 62 individuals provided both genetic and functional imaging data using the Hayling sentence completion task. Individuals with the BDNF ValVal (presumed risk) genotype (n = 41) showed relatively increased activation of the anterior cingulate cortex in relation to Met carrier individuals (n = 21) during sentence completion conditions versus baseline, against a background of similar levels of task performance. It appeared from further investigation that this relatively increased activation was attributable to a failure to disengage or suppress activation in the high risk ValVal group during the task condition, suggesting that BDNF may contribute to the abnormal default network reported in schizophrenia. These results suggest that this gene affects prefrontal brain function in those at high genetic risk for the disorder, unconfounded by medication effects. BDNF may therefore be one of the heritable factors involved in the development of abnormal prefrontal function in schizophrenia. © 2010 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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