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Effects of TPH2 gene variation and childhood trauma on the clinical and circuit-level phenotype of functional movement disorders
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Effects of TPH2 gene variation and childhood trauma on the clinical and circuit-level phenotype of functional movement disorders
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Effects of TPH2 gene variation and childhood trauma on the clinical and circuit-level phenotype of functional movement disorders
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Journal Article
Effects of TPH2 gene variation and childhood trauma on the clinical and circuit-level phenotype of functional movement disorders
2020
Overview
BackgroundFunctional movement disorders (FMDs), part of the wide spectrum of functional neurological disorders (conversion disorders), are common and often associated with a poor prognosis. Nevertheless, little is known about their neurobiological underpinnings, particularly with regard to the contribution of genetic factors. Because FMD and stress-related disorders share a common core of biobehavioural manifestations, we investigated whether variants in stress-related genes also contributed, directly and interactively with childhood trauma, to the clinical and circuit-level phenotypes of FMD.MethodsSixty-nine patients with a ‘clinically defined’ diagnosis of FMD were genotyped for 18 single-nucleotide polymorphisms (SNPs) from 14 candidate genes. FMD clinical characteristics, psychiatric comorbidity and symptomatology, and childhood trauma exposure were assessed. Resting-state functional connectivity data were obtained in a subgroup of 38 patients with FMD and 38 age-matched and sex-matched healthy controls. Amygdala–frontal connectivity was analysed using a whole-brain seed-based approach.ResultsAmong the SNPs analysed, a tryptophan hydroxylase 2 (TPH2) gene polymorphism—G703T—significantly predicted clinical and neurocircuitry manifestations of FMD. Relative to GG homozygotes, T carriers were characterised by earlier FMD age of onset and decreased connectivity between the right amygdala and the middle frontal gyrus. Furthermore, the TPH2 genotype showed a significant interaction with childhood trauma in predicting worse symptom severity.ConclusionsThis is, to our knowledge, the first study showing that the TPH2 genotype may modulate FMD both directly and interactively with childhood trauma. Because both this polymorphism and early-life stress alter serotonin levels, our findings support a potential molecular mechanism modulating FMD phenotype.
Publisher
BMJ Publishing Group Ltd,BMJ Publishing Group LTD,BMJ Publishing Group
Subject
/ Adult Survivors of Child Adverse Events
/ Adverse childhood experiences
/ Amygdala
/ Anxiety
/ Brain-derived neurotrophic factor
/ Conversion Disorder - etiology
/ Conversion Disorder - genetics
/ Conversion Disorder - physiopathology
/ Female
/ Gene-Environment Interaction
/ Genes
/ Genetic Predisposition to Disease - genetics
/ Humans
/ Male
/ Movement Disorders - etiology
/ Movement Disorders - genetics
/ Movement Disorders - physiopathology
/ Polymorphism, Single Nucleotide - genetics
/ Prefrontal Cortex - physiopathology
/ Psychiatric Status Rating Scales
/ Stress
/ Studies
/ Trauma
