Polygenic Risk For Neuroticism Moderates Response To Gains and Losses In Amygdala And Caudate: Evidence From A Clinical Cohort
Autor: | Rayus Kuplicki, Hung-Wen Yeh, Katherine L Forthman, Martin P. Paulus, Tulsa Investigators, Heekyeong Park, Teresa A. Victor, Wesley K. Thompson |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Multifactorial Inheritance
media_common.quotation_subject Precuneus PRS Amygdala Medical and Health Sciences Article Tulsa 1000 Investigators 03 medical and health sciences 0302 clinical medicine Sensitivity Polygenic risk score Reward Clinical Research mental disorders Behavioral and Social Science medicine Genetics 2.1 Biological and endogenous factors Humans Valence (psychology) Aetiology media_common Psychiatry Neuroticism Depression Addiction fMRI Psychology and Cognitive Sciences Neurosciences Anxiety Disorders Magnetic Resonance Imaging 030227 psychiatry Brain Disorders Psychiatry and Mental health Clinical Psychology medicine.anatomical_structure Mood Mental Health Good Health and Well Being Anxiety medicine.symptom Psychology Insula psychological phenomena and processes 030217 neurology & neurosurgery Clinical psychology |
Zdroj: | J Affect Disord |
Popis: | Background Neuroticism is a heritable trait that contributes to the vulnerability to depression. We used polygenic risk scores (PRS) to examine genetic vulnerability to neuroticism and its associations with reward/punishment processing in a clinical sample with mood, anxiety, and substance use disorders. It was hypothesized that higher PRS for neuroticism is associated with attenuated neural responses to reward/punishment. Method Four hundred sixty-nine participants were genotyped and their PRSs for neuroticism were computed. Associations between PRS for neuroticism and anticipatory processing of monetary incentives were examined using functional magnetic resonance imaging. Results Individuals with higher PRS for neuroticism showed less anticipatory activation in the left amygdala and caudate region to incentives regardless of incentive valence. Further, these individuals exhibited altered sensitivity to gain/loss processing in the right anterior insula. Higher PRSs for neuroticism were also associated with reduced processing of gains in the precuneus. Limitations The study population consisted of a transdiagnostic sample with dysfunctions in positive and negative valence processing. PRS for neuroticism may be correlated with current clinical symptoms due to the vulnerability to psychiatric disorders. Conclusions Greater genetic loading for neuroticism was associated with attenuated anticipatory responsiveness in reward/punishment processing with altered sensitivity to valences. Thus, a higher genetic risk for neuroticism may limit the degree to which positive and/or negative outcomes influence the current mood state, which may contribute to the development of positive and negative affective dysfunctions in individuals with mood, anxiety, and addictive disorders. |
Databáze: | OpenAIRE |
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