Background: Neuropsychological abnormalities have been proposed to contribute to the development and maintenance of Borderline Personality Disorder (BPD). Previous meta-analyses and reviews confirmed deficits in a broad range of cognitive domains, including attention, cognitive flexibility, memory, executive functions, planning, information processing, and visuospatial abilities, often suggested to underlie brain abnormalities. However, no study directly explored the structural neural correlates of these deficits in BPD, also accounting for the possible confounding effect of pharmacological treatments, often used as adjunctive symptom-targeted therapy in clinical setting.
View Article and Find Full Text PDFBackground And Objectives: Current studies on emotional dysregulation in BPD suggest that it might be manifested by altered appraisal and biased attentional mechanisms, rather than by hyperreactivity. The aim of this study was to acquire more evidence on this topic by testing the hypothesis that BPD patients are characterized by a negative evaluation bias and reduced visual exploration in response to socio-emotional content. Moreover, the association between the previous conceptualizations and typical dysfunctional processes in BPD were evaluated.
View Article and Find Full Text PDFThe interaction between biological and environmental factors (especially adverse childhood experiences, ACEs) plays a crucial role in the development and maintenance of borderline personality disorder (BPD). These factors act influencing BPD core features such as pervasive instability in affect regulation, impulse control, social cognition, and interpersonal relationships. In line with this perspective, abnormalities in social cognition and related neurobiological underpinnings could mediate the relationship between ACEs and psychopathological manifestations in adulthood.
View Article and Find Full Text PDFUnlabelled: Although HAART suppresses HIV replication, it is often unable to restore immune homeostasis. Consequently, non-AIDS-defining diseases are increasingly seen in treated individuals. This is attributed to persistent virus expression in reservoirs and to cell activation.
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