Social cognition in youth with a first-degree relative with schizophrenia: A systematic scoping review

Social cognition refers to the skills required to recognize, understand, and respond appropriately to others’ intentions and behaviors (Green et al., 2008). Current evidence shows that people with schizophrenia have considerable impairments in social cognition, with deficits consistently observed in facial emotion recognition and theory of mind (Gao et al., 2021; Mondragón-Maya et al., 2017). Some studies have also reported impairments in attributional style and emotion regulation (Aakre et al., 2009; Achim et al., 2016; O'Driscoll et al., 2014; Ludwig et al., 2019). As social cognition is crucial for maintaining interpersonal relationships and employment, impairments in these domains have detrimental effects on daily functioning for those living with schizophrenia (Fett et al., 2011; Green et al., 2015). These deficits tend to remain stable throughout the course of the illness, from the prodromal period to remission (Bowie and Harvey, 2006; Pinkham, 2014). The prodromal period can be defined as the period of time between the appearance of initial abnormal changes and the onset of the first episode of psychosis (Larson et al., 2010).

The stability of social-cognitive deficits raises the possibility that these impairments are trait-like rather than state-like and related to genetic vulnerability for schizophrenia (Lavoie et al., 2013). Schizophrenia is a highly heritable disorder. People who have a first-degree relative (i.e., parents, siblings, children) with the illness share approximately 50% of their genes and are therefore at increased risk of also developing schizophrenia (Phillip and Seidman, 2008). This suggests that first-degree relatives may offer insights on the endophenotypic role of social cognition (Lavoie et al., 2013). The presence of a genetic susceptibility for schizophrenia does not necessarily lead to the development of the disorder but can lead to a progression of deficits and behavioral abnormalities over time (Cornblatt, 2002). Full-blown psychosis only occurs in about 10% of first-degree relatives and typically begins in late adolescence or early adulthood (Cornblatt, 2002; St Clair and Lang, 2021). Subclinical signs and symptoms such as changes in cognition, emotions, and behavior can be detected during the prodromal period (Larson et al., 2010). This period is important as it may offer an early warning of impending psychosis. For example, more severe neurocognitive impairments during this period have been found to increase the risk of developing psychosis (Seidman et al., 2016). As the progression to clinical illness is a gradual process, interventions can be implemented well before the onset of psychosis and potentially prevent its continued progression. To begin early intervention, it is crucial to identify risk markers during the prodromal period to identify individuals at risk for the illness (Cornblatt, 2002; Cornblatt and Auther, 2022).

It has been well-documented that first-degree relatives of individuals with schizophrenia display deficits in neurocognitive domains such as executive functioning, attention, and working memory, and these deficits may be linked to the development of schizophrenia (Harave et al., 2017; Erlenmeyer-Kimling et al., 1995; Weintraub, 1987). For example, the Stony Brook High-Risk Project studied children whose parents had been diagnosed with schizophrenia and found that these children displayed neurocognitive impairments (Weintraub, 1987). Neurocognition was also the focus of the New York High-Risk Study, which determined that attention deficits in children are a promising behavioral marker of schizophrenia (Erlenmeyer-Kimling et al., 1995). High-risk studies have provided strong evidence that in individuals with a biological susceptibility for schizophrenia, impaired neurocognition precedes behavioral disturbances.

Most of the research on the cognitive risk markers for schizophrenia has focused on neurocognition, but research on social cognition in this context is more limited. Additionally, although neurocognition and social cognition are correlated, they are distinct domains (Deckler et al., 2018). Growing evidence suggests that first-degree relatives of individuals with schizophrenia exhibit deficits in social cognition, although less severe than those observed in people with schizophrenia (Ay et al., 2016; Eack et al., 2010; Keshavan et al., 2010). More specifically, first-degree relatives tend to display impairments in facial emotion recognition and theory of mind tasks compared to people without a first-degree relative with schizophrenia (Ay et al., 2016; Horton et al., 2017). There is also some evidence that first-degree relatives of individuals with schizophrenia display an attributional bias compared to control participants (Kumar et al., 2020), as well as difficulties with emotion regulation (Albacete et al., 2016). They also show abnormal neural processing during social cognition tasks (Kozhuharova et al., 2020). In sum, these findings suggest that impairments in social cognition in first-degree relatives may be associated with a genetic vulnerability for schizophrenia (Lemvigh et al., 2022).

Less is known about the extent to which impairments in social cognition are related to symptoms that can indicate the transition to psychosis in youth at FHR (Eack et al., 2010). A meta-analysis on individuals at ultra-high-risk for schizophrenia suggested that some aspects of social cognition, such as emotion recognition and verbal theory of mind may have predictive value for the transition to psychosis; however, there is limited research investigating this in youth at FHR (van Donkersgoed et al., 2015). A recent study observed that youth at FHR who later developed a psychotic disorder had significantly lower emotion recognition performance at baseline and altered amygdala shape over time compared to those who did not convert to psychosis (Guimond et al., 2022). Addressing social-cognitive impairments could therefore be an important focus for early intervention.

Although many studies on social cognition in first-degree relatives of individuals with schizophrenia have contributed to an understanding of the genetic underpinnings of schizophrenia, most focus primarily on first-degree adult relatives over age 35 who are not necessarily at high-risk of developing schizophrenia given their age (Keshavan et al., 2010). Symptoms of schizophrenia, including impairments in social cognition, tend to emerge before age 35 (Gogtay et al., 2011; Rajji et al., 2009). To date, there has been no attempt to synthesize the literature on the social-cognitive profiles specifically among first-degree relatives of individuals with schizophrenia who are younger than 35 years old. Previous reviews and meta-analyses of studies with first-degree relatives of individuals with schizophrenia have included adults who already passed this window of risk without developing schizophrenia (Agnew-Blais and Seidman, 2013; Bora and Pantelis, 2013; Kozhuharova et al., 2020; Lavoie et al., 2013; Martin et al., 2020; Mondragón-Maya et al., 2017). Therefore, there is a need for a new review that synthesizes studies of adolescents and young adults at FHR to better understand how social-cognitive deficits may represent an endophenotype of schizophrenia. Studying whether deficits in social cognition are present in people at FHR who are within these ages of peak risk can provide greater insight into social cognition deficits prior to the typical age of onset for schizophrenia and how these deficits may predict the transition to psychosis. Furthermore, there is currently no review that examines how social-cognitive deficits in youth at FHR are associated with brain correlates and prodromal symptoms of schizophrenia, which could also mark the transition to psychosis. It is crucial to identify these risk markers early in the prodromal phase, as this is a key period to implement interventions that can delay the onset of the illness, reduce symptom severity, and improve long-term outcomes (Hormozpour et al., 2016).

The current review aims to fill these gaps by summarizing the evidence on the differences in social cognition between youth with a first-degree relative with schizophrenia and youth with no familial history of schizophrenia. Our secondary objectives are to explore the brain correlates of social cognition in youth at FHR and the association of social cognition with prodromal symptoms. We anticipate that across the existing literature, youth at FHR will exhibit lower social-cognitive performance in comparison to control groups and that these deficits will be associated with brain abnormalities and prodromal symptoms of schizophrenia.

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