BDNF Val66Met Polymorphism Is Associated with Self-Reported Empathy
نویسندگان
چکیده
Empathy is an important driver of human social behaviors and presents genetic roots that have been studied in neuroimaging using the intermediate phenotype approach. Notably, the Val66Met polymorphism of the Brain-derived neurotrophic factor (BDNF) gene has been identified as a potential target in neuroimaging studies based on its influence on emotion perception and social cognition, but its impact on self-reported empathy has never been documented. Using a neurogenetic approach, we investigated the association between the BDNF Val66Met polymorphism and self-reported empathy (Davis' Interpersonal Reactivity Index; IRI) in a sample of 110 young adults. Our results indicate that the BDNF genotype is significantly associated with the linear combination of the four facets of the IRI, one of the most widely used self-reported empathy questionnaire. Crucially, the effect of BDNF Val66Met goes beyond the variance explained by two polymorphisms of the oxytocin transporter gene previously associated with empathy and its neural underpinnings (OXTR rs53576 and rs2254298). These results represent the first evidence suggesting a link between the BDNF gene and self-reported empathy and warrant further studies of this polymorphism due to its potential clinical significance.
منابع مشابه
Symptom Dimensions and Brain-Derived Neurotrophic Factor Val66Met Polymorphism in Obsessive-compulsive Disorder
Background: Obsessive-Compulsive Disorder (OCD) is a serious neuropsychiatric disorder. The clinical prominence of the OCD symptoms dimensions and Brain-Derived Neurotrophic Factor (BDNF) Val66Met polymorphism are of significant importance. Objectives: The present study aimed to investigate the symptom dimensions and BDNF val66Met polymorphism genotype in Iranian patients with OCD. Materia...
متن کاملThe BDNF Val66Met polymorphism does not moderate the effect of self-reported physical activity on depressive symptoms in midlife.
The brain-derived neurotrophic factor (BDNF) Val66Met single nucleotide polymorphism may be associated with clinical and subsyndromal depression, but physical activity improves mood and increases BDNF expression. The aim of the study was to examine whether the BDNF polymorphism moderates an effect of physical activity on depressive symptoms. BDNF genotype, physical activity measured by the Paff...
متن کاملPredicting change in symptoms of depression during the transition to university: the roles of BDNF and working memory capacity.
Studies on depression risk emphasize the importance of both cognitive and genetic vulnerability factors. The present study has provided the first examination of whether working memory capacity, the BDNF Val66Met polymorphism, and their interaction predict changes in symptoms of depression during the transition to university. Early in the semester, students completed a self-report measure of dep...
متن کاملCognition, serum BDNF levels, and BDNF Val66Met polymorphism in type 2 diabetes patients and healthy controls
Background and aims Type 2 diabetes (T2DM) is associated with cognitive deficits. However, their pathophysiological mechanisms are still unknown. Recent study suggests that brain-derived neurotrophic factor (BDNF) is correlated with cognitive deficits in T2DM patients. This study was to determine whether altered serum BDNF levels and cognitive deficits depended on the BDNF Val66Met polymorphism...
متن کاملThe BDNF Val66Met polymorphism affects HPA-axis reactivity to acute stress.
BACKGROUND Growing evidence suggests that individual differences in HPA-axis reactivity to psychosocial stress are partly due to heritable influences. However, knowledge about the role of specific genetic variants remains very limited to date. Since brain-derived neurotrophic factor (BDNF) not only exhibits neurotrophic actions but is also involved in the regulation of hypothalamic neuropeptide...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره 11 شماره
صفحات -
تاریخ انتشار 2016