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.

人类的社会大脑是复杂的。当前的知识未能定义社会行为所涉及的神经生物学过程，这些过程涉及将系统级现象与脑功能的多个层次联系起来的（病理）生理机制。不幸的是，如此高的复杂性也可能与对几种病原性干预措施的高度敏感性有关。始终如一地，社会缺陷有时代表许多神经精神疾病的最初征兆，包括精神分裂症（SCZ），阿尔茨海默氏病（AD）和重度抑郁症（MDD），这些疾病会导致进行性社会功能障碍。在本综述中，我们总结了将神经生物学底物维持在主要精神疾病中的维持社会功能，社会功能障碍和社会退缩的知识。有趣的是，AD，SCZ，MDD以类似的方式影响社交大脑。因此，社交功能障碍及其最明显的临床表现（即社交退缩）可能代表了创新的转诊领域，从靶向治疗的角度来看，在生物学根源上有可能成为一个独立的实体。