Social brain, social dysfunction and social withdrawal
•The human brain shows several levels of specialization for social stimuli processing.•Social brain could be affected by several neuropsychiatric disorders.•Mechanisms underlying social dysfunction are largely similar across disorders.•Social dysfunction and social withdrawal may represent a transdi...
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| Published in | Neuroscience and biobehavioral reviews Vol. 97; pp. 10 - 33 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Ltd
01.02.2019
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| Subjects | |
| Online Access | Get full text |
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| Abstract | •The human brain shows several levels of specialization for social stimuli processing.•Social brain could be affected by several neuropsychiatric disorders.•Mechanisms underlying social dysfunction are largely similar across disorders.•Social dysfunction and social withdrawal may represent a transdiagnostic domain.•A better understanding of their biological underpinnings may lead to new treatments.
The human social brain is complex. Current knowledge fails to define the neurobiological processes underlying social behaviour involving the (patho-) physiological mechanisms that link system-level phenomena to the multiple hierarchies of brain function. Unfortunately, such a high complexity may also be associated with a high susceptibility to several pathogenic interventions. Consistently, social deficits sometimes represent the first signs of a number of neuropsychiatric disorders including schizophrenia (SCZ), Alzheimer’s disease (AD) and major depressive disorder (MDD) which leads to a progressive social dysfunction. In the present review we summarize present knowledge linking neurobiological substrates sustaining social functioning, social dysfunction and social withdrawal in major psychiatric disorders. Interestingly, AD, SCZ, and MDD affect the social brain in similar ways. Thus, social dysfunction and its most evident clinical expression (i.e., social withdrawal) may represent an innovative transdiagnostic domain, with the potential of being an independent entity in terms of biological roots, with the perspective of targeted interventions. |
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| AbstractList | The human social brain is complex. Current knowledge fails to define the neurobiological processes underlying social behaviour involving the (patho-) physiological mechanisms that link system-level phenomena to the multiple hierarchies of brain function. Unfortunately, such a high complexity may also be associated with a high susceptibility to several pathogenic interventions. Consistently, social deficits sometimes represent the first signs of a number of neuropsychiatric disorders including schizophrenia (SCZ), Alzheimer's disease (AD) and major depressive disorder (MDD) which leads to a progressive social dysfunction. In the present review we summarize present knowledge linking neurobiological substrates sustaining social functioning, social dysfunction and social withdrawal in major psychiatric disorders. Interestingly, AD, SCZ, and MDD affect the social brain in similar ways. Thus, social dysfunction and its most evident clinical expression (i.e., social withdrawal) may represent an innovative transdiagnostic domain, with the potential of being an independent entity in terms of biological roots, with the perspective of targeted interventions.The human social brain is complex. Current knowledge fails to define the neurobiological processes underlying social behaviour involving the (patho-) physiological mechanisms that link system-level phenomena to the multiple hierarchies of brain function. Unfortunately, such a high complexity may also be associated with a high susceptibility to several pathogenic interventions. Consistently, social deficits sometimes represent the first signs of a number of neuropsychiatric disorders including schizophrenia (SCZ), Alzheimer's disease (AD) and major depressive disorder (MDD) which leads to a progressive social dysfunction. In the present review we summarize present knowledge linking neurobiological substrates sustaining social functioning, social dysfunction and social withdrawal in major psychiatric disorders. Interestingly, AD, SCZ, and MDD affect the social brain in similar ways. Thus, social dysfunction and its most evident clinical expression (i.e., social withdrawal) may represent an innovative transdiagnostic domain, with the potential of being an independent entity in terms of biological roots, with the perspective of targeted interventions. The human social brain is complex. Current knowledge fails to define the neurobiological processes underlying social behaviour involving the (patho-) physiological mechanisms that link system-level phenomena to the multiple hierarchies of brain function. Unfortunately, such a high complexity may also be associated with a high susceptibility to several pathogenic interventions. Consistently, social deficits sometimes represent the first signs of a number of neuropsychiatric disorders including schizophrenia (SCZ), Alzheimer's disease (AD) and major depressive disorder (MDD) which leads to a progressive social dysfunction. In the present review we summarize present knowledge linking neurobiological substrates sustaining social functioning, social dysfunction and social withdrawal in major psychiatric disorders. Interestingly, AD, SCZ, and MDD affect the social brain in similar ways. Thus, social dysfunction and its most evident clinical expression (i.e., social withdrawal) may represent an innovative transdiagnostic domain, with the potential of being an independent entity in terms of biological roots, with the perspective of targeted interventions. •The human brain shows several levels of specialization for social stimuli processing.•Social brain could be affected by several neuropsychiatric disorders.•Mechanisms underlying social dysfunction are largely similar across disorders.•Social dysfunction and social withdrawal may represent a transdiagnostic domain.•A better understanding of their biological underpinnings may lead to new treatments. The human social brain is complex. Current knowledge fails to define the neurobiological processes underlying social behaviour involving the (patho-) physiological mechanisms that link system-level phenomena to the multiple hierarchies of brain function. Unfortunately, such a high complexity may also be associated with a high susceptibility to several pathogenic interventions. Consistently, social deficits sometimes represent the first signs of a number of neuropsychiatric disorders including schizophrenia (SCZ), Alzheimer’s disease (AD) and major depressive disorder (MDD) which leads to a progressive social dysfunction. In the present review we summarize present knowledge linking neurobiological substrates sustaining social functioning, social dysfunction and social withdrawal in major psychiatric disorders. Interestingly, AD, SCZ, and MDD affect the social brain in similar ways. Thus, social dysfunction and its most evident clinical expression (i.e., social withdrawal) may represent an innovative transdiagnostic domain, with the potential of being an independent entity in terms of biological roots, with the perspective of targeted interventions. |
| Author | van der Werff, Steven Olivera, Francisco Javier Kas, Martien J. Dukart, Juergen Vorstman, Jacob Posadas, Mar Bilderbeck, Amy Kozak, Rouba Van Der Wee, Nic Glennon, Jeffrey C. Ikram, Arfan Saris, Ilja van Heukelum, Sabrina Lobo, Antonio Lobo, Elena Porcelli, Stefano Serretti, Alessandro Arce, Estibaliz Aghajani, Moji Mogavero, Floriana |
| Author_xml | – sequence: 1 givenname: Stefano orcidid: 0000-0003-0832-8759 surname: Porcelli fullname: Porcelli, Stefano email: stefano.porcelli5@unibo.it organization: Department of Biomedical and NeuroMotor Sciences, University of Bologna, Italy – sequence: 2 givenname: Nic surname: Van Der Wee fullname: Van Der Wee, Nic organization: Leiden Institute for Brain and Cognition/Psychiatric Neuroimaging, Department of Psychiatry, Leiden University Medical Center, the Netherlands – sequence: 3 givenname: Steven surname: van der Werff fullname: van der Werff, Steven organization: Leiden Institute for Brain and Cognition/Psychiatric Neuroimaging, Department of Psychiatry, Leiden University Medical Center, the Netherlands – sequence: 4 givenname: Moji surname: Aghajani fullname: Aghajani, Moji organization: VU University Medical Center, Department of Psychiatry, Amsterdam, the Netherlands – sequence: 5 givenname: Jeffrey C. surname: Glennon fullname: Glennon, Jeffrey C. organization: Donders Institute for Brain, Cognition and Behaviour, Department of Cognitive Neuroscience, Radboud University, the Netherlands – sequence: 6 givenname: Sabrina surname: van Heukelum fullname: van Heukelum, Sabrina organization: Donders Institute for Brain, Cognition and Behaviour, Department of Cognitive Neuroscience, Radboud University, the Netherlands – sequence: 7 givenname: Floriana orcidid: 0000-0003-3249-7544 surname: Mogavero fullname: Mogavero, Floriana organization: Donders Institute for Brain, Cognition and Behaviour, Department of Cognitive Neuroscience, Radboud University, the Netherlands – sequence: 8 givenname: Antonio orcidid: 0000-0002-9098-655X surname: Lobo fullname: Lobo, Antonio organization: Instituto de Investigación Sanitaria de Aragón (IIS Aragón), CIBERSAM, Instituto de Salud Carlos III, Universidad de Zaragoza, Spain – sequence: 9 givenname: Francisco Javier surname: Olivera fullname: Olivera, Francisco Javier organization: Instituto de Investigación Sanitaria de Aragón (IIS Aragón), CIBERSAM, Instituto de Salud Carlos III, Universidad de Zaragoza, Spain – sequence: 10 givenname: Elena surname: Lobo fullname: Lobo, Elena organization: Instituto de Investigación Sanitaria de Aragón (IIS Aragón), CIBERSAM, Instituto de Salud Carlos III, Universidad de Zaragoza, Spain – sequence: 11 givenname: Mar orcidid: 0000-0002-9935-8867 surname: Posadas fullname: Posadas, Mar organization: Instituto de Investigación Sanitaria de Aragón (IIS Aragón), CIBERSAM, Instituto de Salud Carlos III, Universidad de Zaragoza, Spain – sequence: 12 givenname: Juergen surname: Dukart fullname: Dukart, Juergen organization: F. Hoffmann-La Roche, Pharma Research Early Development, Roche Innovation Centre Basel, Basel, Switzerland – sequence: 13 givenname: Rouba surname: Kozak fullname: Kozak, Rouba organization: Neuroscience Research Unit, Global Research & Development, Pfizer Inc., UK – sequence: 14 givenname: Estibaliz surname: Arce fullname: Arce, Estibaliz organization: Neuroscience Research Unit, Global Research & Development, Pfizer Inc., UK – sequence: 15 givenname: Arfan surname: Ikram fullname: Ikram, Arfan organization: Department of Epidemiology, Erasmus University Medical Center Rotterdam, the Netherlands – sequence: 16 givenname: Jacob orcidid: 0000-0002-1677-3126 surname: Vorstman fullname: Vorstman, Jacob organization: Kinder-en jeugdpsychiater & onderzoeker, Divisie Hersenen, Psychiatrie, Universitair Medisch Centrum Utrecht, the Netherlands – sequence: 17 givenname: Amy surname: Bilderbeck fullname: Bilderbeck, Amy organization: P1vital Ltd., UK – sequence: 18 givenname: Ilja orcidid: 0000-0003-3970-5123 surname: Saris fullname: Saris, Ilja organization: VU University Medical Center, Department of Psychiatry, Amsterdam, the Netherlands – sequence: 19 givenname: Martien J. orcidid: 0000-0002-4471-8618 surname: Kas fullname: Kas, Martien J. organization: Groningen Institute for Evolutionary Life Sciences, University of Groningen, the Netherlands – sequence: 20 givenname: Alessandro orcidid: 0000-0003-4363-3759 surname: Serretti fullname: Serretti, Alessandro organization: Department of Biomedical and NeuroMotor Sciences, University of Bologna, Italy |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30244163$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Alzheimer’s disease Major depression disorder Neurobiology Schizophrenia Social brain Social cognition Social dysfunction Social functioning Social impairments Social withdrawal |
| Title | Social brain, social dysfunction and social withdrawal |
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