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Maternal Postnatal Psychopathology Predicts Identity Diffusion in Young Adult Offspring.
Children (Basel)
December 2024
Department of Child and Adolescent Psychiatry, Saarland University Hospital, 66421 Homburg, Germany.
Background/objectives: In the new conceptualization of personality disorders (PD) in ICD-11 and Diagnostic and Statistical Manual 5 Alternative Model of Personality Disorders (DSM-5 AMPD), identity development in terms of impaired personality functioning plays a central role in diagnostic guidelines and determining PD severity. On the one hand, there is a temporary identity crisis while keeping an integrated sense of identity and, on the other hand, there is pathological identity diffusion, which is associated with a high risk of a current or emerging PD. The latter is characteristic not only of borderline PD but of all personality disorders and should be detected as early as possible to prevent chronic illness and critical life courses.
View Article and Find Full Text PDFExploring the bidirectional causality between neuroticism and frailty: a Mendelian randomization analysis.
Hereditas
January 2025
Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou, China.
Background: Epidemiological studies have confirmed the relationship between personality trait neuroticism and physical health. However, the relationship between neuroticism and frailty remains unconfirmed. This study employed a bi-directional two-sample Mendelian randomization (MR) approach to investigate the causal relationship between neuroticism and frailty.
View Article and Find Full Text PDFAntisocial personality disorder:Failure to balance excitation/inhibition?
Neuropharmacology
January 2025
Division of Molecular Psychiatry, Center of Mental Health, University Hospital Würzburg, Würzburg, Germany; Department of Psychiatry, Psychosomatics and Psychotherapy, Center of Mental Health, University Hospital Würzburg, Würzburg, Germany.
While healthy brain function relies on a dynamic but tightly regulated interaction between excitation (E) and inhibition (I), a spectrum of social cognition disorders, including antisocial behavior and antisocial personality disorder (ASPD), frequently ensuing from irregular neurodevelopment, may be associated with E/I imbalance and concomitant alterations in neural connectivity. Technological advances in the evaluation of structural and functional E/I balance proxies in clinical settings and in human cell culture models provide a general basis for identification of biomarkers providing a powerful concept for prevention and intervention across different dimensions of mental health and disease. In this perspective we outline a framework for research to characterize neurodevelopmental pathways to antisocial behavior and ASPD driven by (epi)genetic factors across life, and to identify molecular targets for preventing the detrimental effects of cognitive dysfunction and maladaptive social behavior, considering psychosocial experience; to validate signatures of E/I imbalance and altered myelination proxies as biomarkers of pathogenic neural circuitry mechanisms to determine etiological processes in the transition from mental health to antisocial behavior and ASPD and in the switch from prevention to treatment; to develop a neurobiologically-grounded integrative model of antisocial behavior and ASPD resultant of disrupted E/I balance, allowing to establish objective diagnoses and monitoring tools, to personalize prevention and therapeutic decisions, to predict treatment response, and thus counteract relapse; and finally, to promote transformation of dimensional disorder taxonomy and to enhance societal awareness and reception of the neurobiological basis of antisocial behavior and ASPD.
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