Aims: Autism spectrum disorder and schizophrenia are traditionally viewed as distinct diagnostic categories. However, evidence increasingly suggests overlapping pathological functioning at various levels, starting from brain circuitry to behaviour. Notably, both disorders are characterized by anomalous minimal self-experience (altered body ownership and agency), which is a trait-like, phenomenological distortion. We propose a conceptual framework that unites multiple levels, from neural mechanisms to cognitive and phenomenological correlates, for understanding minimal self-disturbance across diagnostic boundaries.
Methods: A comprehensive review of existing literature was conducted, examining phenomenological, neurocognitive, and neural correlates of minimal self-disturbance in both schizophrenia and autism spectrum disorder. Assessment tools and scales such as the Examination of Anomalous Self-Experience Scale, as well as experimental neurocognitive paradigms like the Rubber-Hand Illusion and self-relevant stimuli tasks, were examined for their relevance in evaluating self-experience in both conditions.
Results: Minimal self-disturbances were found to be a prominent feature of both schizophrenia and autism, albeit with different manifestations. Patients with schizophrenia showed heightened susceptibility to body ownership alterations, while individuals with autism exhibited decreased susceptibility. Neural markers, particularly within the default mode network and thalamocortical connectivity, were implicated in self-disturbance in both disorders, suggesting a shared neurobiological basis.
Conclusion: The minimal self- disturbance appears to be a transdiagnostic feature of both schizophrenia and autism spectrum disorder, indicating that these conditions may represent points along a shared psychopathological continuum. The proposed model integrates neurobiological, cognitive, and phenomenological aspects of self-disturbance, offering a comprehensive framework for understanding and assessing disruptions in self-experience across these conditions. This approach promotes a shift away from rigid diagnostic classifications towards approaches that highlight the importance of atypical self-experience. (Neuropsychopharmacol Hung 2024; 26(4): 218-226)
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Neuropsychopharmacol Hung
December 2024
Pszichiátriai és Pszichoterápiás Klinika, Semmelweis Egyetem, Budapest.
Neurosci Biobehav Rev
January 2025
Department of Pharmaceutical Sciences, Faculty of Life Sciences, Gurugram University (A State Govt. University), Gurugram, Haryana, India. Electronic address:
Plexins are a family of transmembrane receptors known for their diverse roles in neural development, axon guidance, neuronal migration, synaptogenesis, and circuit formation. Semaphorins are a class of secreted and membrane proteins that act as primary ligands for plexin receptors. Semaphorins play a crucial role in central nervous system (CNS) development by regulating processes such as axonal growth, neuronal positioning, and synaptic connectivity.
View Article and Find Full Text PDFSchizophr Bull
January 2025
Université Paris Cité, Institute of Psychiatry and Neuroscience of Paris (IPNP), INSERM U1266, Team "Pathophysiology of psychiatric disorders", Institut de psychiatrie, CNRS GDR 3557, 75014 Paris, France.
J Child Psychol Psychiatry
January 2025
National Centre for Register-Based Research (NCRR), Aarhus University, Aarhus, Denmark.
Background: More research is needed to understand psychopathology among parents of children with mental disorders in the years before and after the child is diagnosed. Here, we estimated the risk of mental disorders and psychotropic medication use in parents of children with versus without mental disorders and the temporal associations between child and parental psychopathology.
Methods: We conducted a population-based matched cohort study using Danish register data.
eNeuro
January 2025
Department of Neuroscience, University of Wisconsin-Madison, Madison, WI, 53705
Fragile X autosomal homolog 1 (FXR1), a member of the fragile X messenger riboprotein 1 family, has been linked to psychiatric disorders including autism and schizophrenia. Parvalbumin (PV) interneurons play critical roles in cortical processing, and have been implicated in FXR1-linked mental illnesses. Targeted deletion of FXR1 from PV interneurons in mice has been shown to alter cortical excitability and elicit schizophrenia-like behavior.
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