Social cognition, essential for interpreting and responding to social contexts, is frequently impaired in neurological and psychiatric disorders. Multiple brain regions, organized in large-scale brain networks, represent the neurobiological substrate of social cognitive abilities, and are the main target of neurodegeneration in the fronto-temporal dementia spectrum. The focus of this review is a specific anatomic subcomponent of these networks, i.e. the amygdalo-hippocampal complex (AHC). Animal models suggest that the AHC is involved in processes underlying social cognition through both localized mechanisms and integration within large-scale networks. In humans, AHC pathology in conditions such as Alzheimer’s disease (AD), epilepsy, and autoimmune encephalitis (AIE) has been associated with social cognition impairment. In AD and Mild Cognitive Impairment (MCI) deficits in Theory of Mind (ToM), empathy, and emotion recognition are common and linked to medial temporal atrophy. In focal frontal and temporal lobe epilepsy, seizures and interictal dysfunctions disrupt social cognition, particularly ToM, from early stages. In AIE, marked fear recognition deficits are closely related to amygdala involvement. These conditions highlight the association between social cognition impairments and damage to the AHC. From a theoretical perspective, investigating the relationship between the AHC and social cognition may advance our understanding of the neurobiological underpinnings of social behavior. Clinically, the systematic assessment of social cognition in patients with conditions affecting the AHC appears warranted, potentially improving diagnosis, prognostic evaluation, and therapeutic strategies.
Beyond memories: A narrative review on the role of amygdalo-hippocampal complex in social cognition / Quaranta, D., Scalese, A., Luzzi, S., Cherubini, V., Giovagnoli, A., Cappa, S.F.. - In: NEUROLOGICAL SCIENCES. - ISSN 1590-1874. - 47:(2026). [10.1007/s10072-026-09265-0]
Beyond memories: A narrative review on the role of amygdalo-hippocampal complex in social cognition
Luzzi S.;Cherubini V.;
2026-01-01
Abstract
Social cognition, essential for interpreting and responding to social contexts, is frequently impaired in neurological and psychiatric disorders. Multiple brain regions, organized in large-scale brain networks, represent the neurobiological substrate of social cognitive abilities, and are the main target of neurodegeneration in the fronto-temporal dementia spectrum. The focus of this review is a specific anatomic subcomponent of these networks, i.e. the amygdalo-hippocampal complex (AHC). Animal models suggest that the AHC is involved in processes underlying social cognition through both localized mechanisms and integration within large-scale networks. In humans, AHC pathology in conditions such as Alzheimer’s disease (AD), epilepsy, and autoimmune encephalitis (AIE) has been associated with social cognition impairment. In AD and Mild Cognitive Impairment (MCI) deficits in Theory of Mind (ToM), empathy, and emotion recognition are common and linked to medial temporal atrophy. In focal frontal and temporal lobe epilepsy, seizures and interictal dysfunctions disrupt social cognition, particularly ToM, from early stages. In AIE, marked fear recognition deficits are closely related to amygdala involvement. These conditions highlight the association between social cognition impairments and damage to the AHC. From a theoretical perspective, investigating the relationship between the AHC and social cognition may advance our understanding of the neurobiological underpinnings of social behavior. Clinically, the systematic assessment of social cognition in patients with conditions affecting the AHC appears warranted, potentially improving diagnosis, prognostic evaluation, and therapeutic strategies.| File | Dimensione | Formato | |
|---|---|---|---|
|
Quaranta_Beyond-memories-narrative-review_2026.pdf
accesso aperto
Tipologia:
Versione editoriale (versione pubblicata con il layout dell'editore)
Licenza d'uso:
Creative commons
Dimensione
800.88 kB
Formato
Adobe PDF
|
800.88 kB | Adobe PDF | Visualizza/Apri |
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


