ABSTRACT
OBJECTIVE: A considerable number of adolescents exhibit severe self-regulation deficits in affect and behavior, which are referred to as affective dysregulation (AD). AD may be conceptualized as a dimensional trait that, in its extreme form, resembles the diagnostic categories of severe mood dysregulation (SMD) or disruptive mood dysregulation disorder (DMDD). Assuming a shared pathway of psychopathology in AD and SMD, similar underlying dysfunctional mechanisms in emotion processing, particularly emotion recognition (RECOG) and regulation (REGUL), may be postulated. METHOD: Adolescent inpatients with AD (CAD, N = 35), without AD (CCG, N = 28), and nonclinical controls (NCG; N = 28) were administered a morphed facial recognition task (RECOG). REGUL abilities, levels of irritability as well as depressive symptoms were also assessed. RESULTS: We found no significant group differences in accuracy and thresholds for RECOG abilities. Patients with AD reported more dysfunctional REGUL strategies than did CCG and NCG. Both depression and AD, but not irritability, influenced the overall degree of maladaptive REGUL. CONCLUSION: The broad phenotype of AD does not involve the deficits in RECOG reported for adolescents with a narrow phenotype (SMD); regarding REGUL strategies, AD seems to be associated with specific impairments.
Subject(s)
Affective Symptoms/diagnosis , Affective Symptoms/psychology , Emotional Adjustment , Emotional Intelligence , Mood Disorders/psychology , Adolescent , Attention Deficit Disorder with Hyperactivity/diagnosis , Attention Deficit Disorder with Hyperactivity/psychology , Bipolar Disorder/diagnosis , Bipolar Disorder/psychology , Child , Comorbidity , Diagnosis, Differential , Expressed Emotion , Facial Recognition , Female , Humans , Irritable Mood , Male , Mood Disorders/diagnosis , Personality Assessment/statistics & numerical data , Psychometrics/statistics & numerical data , Reproducibility of Results , Surveys and QuestionnairesABSTRACT
ATAD2 (ANCCA) is an epigenetic regulator and transcriptional cofactor, whose overexpression has been linked to the progress of various cancer types. Here, we report a DNA-encoded library screen leading to the discovery of BAY-850, a potent and isoform selective inhibitor that specifically induces ATAD2 bromodomain dimerization and prevents interactions with acetylated histones in vitro, as well as with chromatin in cells. These features qualify BAY-850 as a chemical probe to explore ATAD2 biology.
