TY - JOUR
T1 - Social brain, social dysfunction and social withdrawal
AU - Porcelli, Stefano
AU - van der Wee, Nic
AU - van der Werff, Steven
AU - Aghajani, Moji
AU - Glennon, Jeffrey C.
AU - van Heukelum, Sabrina
AU - Mogavero, Floriana
AU - Lobo, Antonio
AU - Olivera, Francisco Javier
AU - Lobo, Elena
AU - Posadas, Mar
AU - Dukart, Juergen
AU - Kozak, Rouba
AU - Arce, Estibaliz
AU - Ikram, Arfan
AU - Vorstman, Jacob
AU - Bilderbeck, Amy
AU - Saris, Ilja
AU - Kas, Martien J.
AU - Serretti, Alessandro
PY - 2019/2/1
Y1 - 2019/2/1
N2 - 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.
AB - 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.
KW - Alzheimer's disease
KW - Major depression disorder
KW - Neurobiology
KW - Schizophrenia
KW - Social brain
KW - Social cognition
KW - Social dysfunction
KW - Social functioning
KW - Social impairments
KW - Social withdrawal
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85053865881&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/30244163
U2 - 10.1016/j.neubiorev.2018.09.012
DO - 10.1016/j.neubiorev.2018.09.012
M3 - Review article
C2 - 30244163
SN - 0149-7634
VL - 97
SP - 10
EP - 33
JO - Neuroscience and Biobehavioral Reviews
JF - Neuroscience and Biobehavioral Reviews
IS - 97
ER -