Social Cognitive Impairment Research Articles

Effect of Sleep Hygiene Orientation on Social Cognition Impairments Due to Chronic Sleep Restriction in Mexican Medical Residents

Effect of Sleep Hygiene Orientation on Social Cognition Impairments Due to Chronic Sleep Restriction in Mexican Medical Residents

Searching the underlying mechanisms of specific learning disorder: An emotion recognition and social cognition aspect for Turkish clinical youth population

This study aimed to investigate impairments in social cognition in youth with specific learning disorder (SLD) through a cross sectional study. Eighty six adolescents which include of 43 SLD and 43 typically developing (TD) children completed a battery of tests to analyze social cognition, emotional process and clinical psychopathological profile. SLD group performed significantly worse than healthy controls in facial ER total accuracy score (Cohen d = .77) and Stroop interference (Cohen d = .92). In individual emotion analyses, patients with SLD have a very high deficiency in recognition of angry faces (Cohen d = .89). Between-group difference was also significant for Stroop congruent and facilitation scores (Cohen d = .99). The Specific Learning Disorder Symptom Check List-Parent Form scores were significant –and only- predictor of the model which for total accuracy score of facial recognition. The results of this study supported an impairment in emotion recognition and executive functions in adolescents with SLD but causality seems still unclear.

Association Between Insulin-Like Growth Factor-1 and Social Cognition in Huntington's Disease.

Insulin-like growth factor 1 (IGF-1) seems to be involved in the neural circuits associated with social cognition and brain structure. To investigate the association of IGF-1 levels with social cognition and brain structure in Huntington's disease (HD). We evaluated social cognition using the Ekman test in 22 HD patients and 19 matched controls. Brain structure was assessed using standard volume-based voxel-based morphometry and surface-based cortical thickness pipeline. We analyzed the association of IGF-1 levels with social cognition and brain structure using adjusted regression analysis. Social cognition was worse in HD patients (P < 0.001), on antidopaminergic drugs (P=0.02), and with lower IGF-1 levels (P=0.04). In neuroimaging analyses, lower IGF-1 levels were associated with social cognition impairment and atrophy mainly in frontotemporal regions (P < 0.05 corrected). In HD, abnormal IGF-1 function seems to be associated with brain atrophy leading to clinical deficits in social cognition.

Mild behavioral impairment symptom severity predicts tau hyperphosphorylation assessed by plasma p‐tau181 across the Alzheimer’s disease spectrum

AbstractBackgroundMild behavioral impairment (MBI) is a neurobehavioral syndrome characterized by the emergence of persistent non‐cognitive neuropsychiatric symptoms (NPS) in older adults, representing an at‐risk state for dementia and a potential marker of Alzheimer’s disease (AD). However, few studies have investigated associations between MBI and plasma biomarkers of AD pathophysiology, specifically tau hyperphosphorylation.MethodIndividuals across the AD spectrum (cognitively unimpaired (CU) and impaired (CI)) were selected from the Translational Biomarkers of Aging and Dementia (TRIAD) cohort. MBI was assessed using the MBI‐Checklist (MBI‐C), which assesses NPS severity in five subdomains: decreased motivation (apathy), emotional dysregulation (mood/anxiety symptoms), impulse dyscontrol (agitation, impulsivity, abnormal reward salience), social inappropriateness (impaired social cognition), and abnormal thoughts/perception (psychosis). Plasma levels of p‐tau181 were quantified in all individual, and log‐transformed due to right skew. Spearman correlation analysis investigated cross‐sectional associations between plasma p‐tau181 and MBI‐C scores, and between baseline plasma p‐tau181 and annual change in MBI‐C. Multivariable linear regression analyses assessed the ability of cross‐sectional and longitudinal MBI‐C scores to predict plasma p‐tau181, adjusting for age, sex, education, and diagnostic group (CU/CI, Aβ +/‐).ResultCross‐sectional MBI data were available for 211 individuals, with longitudinal data available for 128 individuals (). Significant correlations were found between plasma p‐tau181 and MBI‐C total and apathy scores in the cross‐sectional sample (Figure A). Further, significant correlations were found with plasma p‐tau181 and the annual change in MBI‐C total and apathy scores (Figure B). These associations were corroborated by significant standardized and adjusted regression coefficients from multivariate regression models, which showed that baseline and longitudinal MBI‐C total and apathy score predicted plasma level of p‐tau181 (Figure C).ConclusionOur study provides novel findings on the association between MBI and tau hyperphosphorylation assessed using plasma biomarkers in an AD cohort. These results add to the existing evidence for MBI as a clinical manifestation of AD pathology and support the use of the MBI‐C as an enrichment tool for clinical trial enrollment and therapeutic intervention.

Examining the Moderating Roles of Social Isolation and Social Technology Use in Health Disparities of Cognitive Impairment

AbstractBackgroundThere are profound racial disparities in cognitive impairment and dementia. Black and rural older adults are nearly twice as likely to develop dementia compared to White and urban‐dwelling older adults, respectively. However, the way social factors affect these racial and rural‐urban disparities in dementia prevalence remains poorly understood. Social isolation is associated with poorer cognitive outcomes among older adults, yet social technology use may provide a means to reduce social isolation. This research examines how two social factors—social isolation and social technology use influence racial and rural disparities in cognitive impairment and dementia.MethodData was extracted from the 2014 to 2018 waves of the Health and Retirement Study (N = 5,358). Participants (aged 50‐102) completed survey measures of social isolation, loneliness, and frequency of online social communication (e.g., use of Facebook, Skype). The modified Telephone Interview for Cognitive Status was used to operationalize dementia. The validated TICS classification system was used to classify scores with a cognitive status of dementia (scores ≤6), cognitive impairment (score of 7‐11), or cognitively normal (scores ≥12). Data was analyzed using structural equation models.ResultAcross all groups, frequency of social technology use moderated the negative relationship between social isolation and cognitive impairment, controlling for age, education, gender, wealth, and general computer usage. More frequent social technology use was associated with cognitively normal status among older adults who reported greater degrees of social isolation. In terms of health disparities, the results revealed racial, but not rural‐urban, differences in the relationship between frequency of social technology use and cognitive status. Frequent social technology use was associated with improved cognitive status in Black American older adults but not White older adults, irrespective of their level of social isolation.ConclusionSocial technology may offer a means to mitigate cognitive decline; the potential benefit of such technology may be particularly promising among Black older adults.

Psychopathic and autistic traits differentially influence the neural mechanisms of social cognition from communication signals

Psychopathy is associated with severe deviations in social behavior and cognition. While previous research described such cognitive and neural alterations in the processing of rather specific social information from human expressions, some open questions remain concerning central and differential neurocognitive deficits underlying psychopathic behavior. Here we investigated three rather unexplored factors to explain these deficits, first, by assessing psychopathy subtypes in social cognition, second, by investigating the discrimination of social communication sounds (speech, non-speech) from other non-social sounds, and third, by determining the neural overlap in social cognition impairments with autistic traits, given potential common deficits in the processing of communicative voice signals. The study was exploratory with a focus on how psychopathic and autistic traits differentially influence the function of social cognitive and affective brain networks in response to social voice stimuli. We used a parametric data analysis approach from a sample of 113 participants (47 male, 66 female) with ages ranging between 18 and 40 years (mean 25.59, SD 4.79). Our data revealed four important findings. First, we found a phenotypical overlap between secondary but not primary psychopathy with autistic traits. Second, primary psychopathy showed various neural deficits in neural voice processing nodes (speech, non-speech voices) and in brain systems for social cognition (mirroring, mentalizing, empathy, emotional contagion). Primary psychopathy also showed deficits in the basal ganglia (BG) system that seems specific to the social decoding of communicative voice signals. Third, neural deviations in secondary psychopathy were restricted to social mirroring and mentalizing impairments, but with additional and so far undescribed deficits at the level of auditory sensory processing, potentially concerning deficits in ventral auditory stream mechanisms (auditory object identification). Fourth, high autistic traits also revealed neural deviations in sensory cortices, but rather in the dorsal auditory processing streams (communicative context encoding). Taken together, social cognition of voice signals shows considerable deviations in psychopathy, with differential and newly described deficits in the BG system in primary psychopathy and at the neural level of sensory processing in secondary psychopathy. These deficits seem especially triggered during the social cognition from vocal communication signals.

Neuroinflammation Underlies the Development of Social Stress Induced Cognitive Deficit in Sickle Cell Disease

Cognitive deficits have been observed in children and adults with sickle cell disease (SCD), with and without cerebral infarcts. Risk factors include systemic inflammation, neuroinflammation, and severe anemia, and sociological risk factors such as parental education level and income. Additionally, there is a reported relationship between plasma cytokine levels and cognitive function in children with SCD, suggesting a link between inflammation and cognitive deficit in SCD. This study aims to examine the mechanism underlying the development of cognitive deficit in SCD with exposure to social stress, by using the repeat social defeat (RSD) paradigm in sickle cell mice. We hypothesized that neuroinflammation is a major underlying mechanism mediating the relationship between social stress and development of cognitive deficit in SCD. RSD was done by introducing a male intruder mouse (an aggressor) into an established cage of 3, 6 months old male sickle cell or control mice, every day, for two hours, for six consecutive days. Age and sex-matched control (sickle cell and non-sickle cell mice) cages were set up but without aggressor mice. On the seventh day, mice were tested for cognitive/behavioral deficit using novel object recognition (NOR) and fear conditioning (FC) test paradigms. Except for the aggressors, all mice used were Townes humanized sickle cell (SS) and control (AA) mice. To test the hypothesis that neuroinflammation is an underlying mechanism, a second cohort of SS and AA nice were randomly assigned to oral (in drinking water) minocycline treatment (90mg/kg) or placebo (drinking water). Mice within treatment arms were randomly assigned to RSD exposure or no RSD exposure. Minocycline treatment was started one day prior to the day of commencing RSD and terminated on the same day as the final RSD session and the dose was kept constant by adjusting the amount administered daily, using the water consumption from the previous day. Cognitive/behavioral testing was performed as before, starting the next day after day 6 of RSD and day 7 of treatment. Mice were sacrificed 1-2 days after completion of behavioral testing and brains were extracted for histological analysis. Cellular evidence of neuroinflammation in the hippocampus/dentate gyrus was determined using immunohistochemistry to quantify peripheral immune cell infiltrates (CD45+ (bone marrow-derived microglia), CD3+ (T-cell density), B220+ (B-cell density), and Iba1+ (activated microglia). We used Golgi-Cox impregnation to quantify spine density and maturity in cortical and hippocampal pyramidal neurons. There were no differences between 6 months old AA and SS with regards to percent preference on NOR test (53.1 ± 4.4% vs. 56.1 ± 5.6%). However, SS mice exposed to RSD, had a lower percent preference (36.1 ± 6.7%, p = 0.06) for the novel object compared to SS mice not exposed to RSD (56.1 ± 5.6%), indicating the presence of a memory deficit in SS mice exposed to RSD. The SS mice exposed to RSD had worse performance on contextual FC test (p = 0.001), indicated by a lower percent freezing compared with SS mice not exposed to RSD. Additionally, SS mice exposed to RSD also had a higher density of activated microglia (260.2 ± 3.7 vs. 233.6 ± 4.0; p ≤ 0.0001) and bone marrow derived microglia (125.4 ± 6.2 vs. 93.7 ± 5.0; p = 0.0004) in the dentate gyrus, compared to SS mice not exposed to RSD, suggesting increased neuroinflammation after RSD exposure. There were no differences in B or T cell density. SS mice treated with minocycline during RSD exposure showed improvement in memory based on NOR (67.1 ± 4.5% vs 36.1 ± 6.7%, p = 0.0007) and contextual FC (p = 0.01) tests compared to SS mice exposed to RSD and not treated with minocycline. The treated mice had fewer activated microglia (168.4 ± 6.7 vs. 260.2 ± 3.7; p ≤ 0.0001) and bone marrow derived microglia (31.79 ± 2.2 vs. 125.4 ± 6.2; p≤0.0001) in the dentate gyrus compared to the non-treated SS mice exposed to RSD. Additionally, the treated SS mice exposed to RSD also showed increases in neuron progenitor stem cells density improvement in neurogenesis and a decrease in astrogliosis in granular zone of the dentate gyrus, compared to the SS mice exposed to RSD without minocycline treatment. We demonstrate for the first time that neuroinflammation is one of the underlying mechanisms of social stress related cognitive impairment in mice and may be applicable to children with SCD and might be treatable using anti-neuroinflammatory drugs. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

Impairment of social cognitive functions in the patients with acute ischemic stroke

BACKGROUND. Cognitive impairment is common after a stroke. However, the condition of social cognitive functions, in particular theory of mind, in this group of patients has been studied insufficiently.&#x0D; AIM. To study the frequency and predictors of the development of the social cognitive disorders based on theory of mind impairment in patients with acute ischemic stroke.&#x0D; MATERIAL AND METHODS. Theory of mind impairment was assessed using Reading the Mind in the Eyes test in the acute period of ischemic stroke. National Institutes of Health Stroke scale was used to assess the severity of neurological deficit, modified Rankin scale the degree of disability, Delirium Severity Rating Scale the symptoms of delirium, Buss Perry aggressiveness scale severity of aggressive behavior, Montreal Cognitive Assessment Scale cognitive deficit. The severity of cortical atrophy was evaluated by computed tomography of the brain. The study included 86 patients, 53 males and 33 females. The average age of patients was 64 years. Statistical analysis was performed using the IBM SPSS Statistics 21 software package. Nonparametric statistics methods were used. Binary data were compared using the chi-square parameter, categorical data were compared using the MannWhitney test.&#x0D; RESULTS. Seventy percent of patients suffered from the impairment of social cognitive functions. Independent predictors of the impairment of theory of mind according to linear regression analysis were cognitive dysfunction according to the Montreal Cognitive Assessment Scale (p=0.0001) and the severity of cortical atrophy on computed tomography of the brain (p=0.001).&#x0D; CONCLUSION. Social cognitive impairment is registered in a substantial number of patients in acute period of stroke; its predictors include general cognitive impairment and cortical atrophy of the brain.

Social cognition deficits and biometric signatures in the behavioural variant of Alzheimer's disease.

The behavioural variant of Alzheimer's disease (bvAD) is characterized by early predominant behavioural changes, mimicking the behavioural variant of frontotemporal dementia (bvFTD), which is characterized by social cognition deficits and altered biometric responses to socioemotional cues. These functions remain understudied in bvAD. We investigated multiple social cognition components (i.e. emotion recognition, empathy, social norms and moral reasoning), using the Ekman 60 faces test, Interpersonal Reactivity Index, empathy eliciting videos, Social Norms Questionnaire and moral dilemmas, while measuring eye movements and galvanic skin response. We compared 12 patients with bvAD with patients with bvFTD (n = 14), typical Alzheimer's disease (tAD, n = 13) and individuals with subjective cognitive decline (SCD, n = 13), using ANCOVAs and age- and sex-adjusted post hoc testing. Patients with bvAD (40.1 ± 8.6) showed lower scores on the Ekman 60 faces test compared to individuals with SCD (49.7 ± 5.0, P < 0.001), and patients with tAD (46.2 ± 5.3, P = 0.05) and higher scores compared to patients with bvFTD (32.4 ± 7.3, P = 0.002). Eye-tracking during the Ekman 60 faces test revealed no differences in dwell time on the eyes (all P > 0.05), but patients with bvAD (18.7 ± 9.5%) and bvFTD (19.4 ± 14.3%) spent significantly less dwell time on the mouth than individuals with SCD (30.7 ± 11.6%, P < 0.01) and patients with tAD (32.7 ± 12.1%, P < 0.01). Patients with bvAD (11.3 ± 4.6) exhibited lower scores on the Interpersonal Reactivity Index compared with individuals with SCD (15.6 ± 3.1, P = 0.05) and similar scores to patients with bvFTD (8.7 ± 5.6, P = 0.19) and tAD (13.0 ± 3.2, P = 0.43). The galvanic skin response to empathy eliciting videos did not differ between groups (all P > 0.05). Patients with bvAD (16.0 ± 1.6) and bvFTD (15.2 ± 2.2) showed lower scores on the Social Norms Questionnaire than patients with tAD (17.8 ± 2.1, P < 0.05) and individuals with SCD (18.3 ± 1.4, P < 0.05). No group differences were observed in scores on moral dilemmas (all P > 0.05), while only patients with bvFTD (0.9 ± 1.1) showed a lower galvanic skin response during personal dilemmas compared with SCD (3.4 ± 3.3 peaks per min, P = 0.01). Concluding, patients with bvAD showed a similar although milder social cognition profile and a similar eye-tracking signature to patients with bvFTD and greater social cognition impairments and divergent eye movement patterns compared with patients with tAD. Our results suggest reduced attention to salient facial features in these phenotypes, potentially contributing to their emotion recognition deficits.

Theory of mind and facial emotion recognition in adults with temporal lobe epilepsy: A meta-analysis.

BackgroundMounting studies have investigated impairments in social cognitive domains (including theory of mind [ToM] and facial emotion recognition [FER] in adult patients with temporal lobe epilepsy (TLE). However, to date, inconsistent findings remain.MethodsA search of PubMed, Web of Science, and Embase databases was conducted until December 2021. Hedges g effect sizes were computed with a random-effects model. Meta-regressions were used to assess the potential confounding factors of between-study variability in effect sizes.ResultsThe meta-analysis included 41 studies, with a combined sample of 1,749 adult patients with TLE and 1,324 healthy controls (HCs). Relative to HCs, adult patients with TLE showed large impairments in ToM (g = −0.92) and cognitive ToM (g = −0.92), followed by medium impairments in affective ToM (g = −0.79) and FER (g = −0.77). Besides, no (statistically) significant differences were observed between the magnitude of social cognition impairment in adult with TLE who underwent and those who did not undergo epilepsy surgery. Meta-regressions exhibited that greater severity of executive functioning was associated with more severe ToM defects, and older age was associated with more severe FER defects.ConclusionsResults of this meta-analysis suggest that adult patients with TLE show differential impairments in the core aspects of social cognitive domains (including ToM and FER), which may help in planning individualized treatment with appropriate cognitive and behavioral interventions.

GIGYF1-disturbed IGF-1R recycling: a potential contributor to autism spectrum disorder pathogenesis?

Autism spectrum disorder (ASD) is a highly variable and heritable neurodevelopmental disease (NDD) with strong genetic underpinnings. In this issue of the JCI, Chen et al. analyzed 2 previously reported, large-scale sequenced ASD cohorts and reported that GIGYF1 is the second most mutated among ASD risk genes. In this issue of the JCI, Chen et al. used a conditional mouse model combined with molecular technologies based on human genetic analyses to determine the critical role of GIGYF1 in ASD. GIGYF1-deficiency affected the recycling of IGF-1R, thereby suppressing the IGF-1R/ERK signaling pathway. Disruption of GIGYF1 in the developing mouse brain led to social deficits and cognitive impairments. These findings extend our understanding of ASD pathogenesis and provide an avenue for developing potentially effective preventions and treatments for patients with ASD.

Von Economo Neuron Involvement in Social Cognitive and Emotional Impairments in Neuropsychiatric Disorders.

Von Economo Neuron Involvement in Social Cognitive and Emotional Impairments in Neuropsychiatric Disorders.

Comprehension of core grammar in diverse samples of Mandarin-acquiring preschool children with ASD

Abstract In this review, we summarize studies investigating comprehension of three core grammatical structures (Subject-Verb-Object word order, grammatical aspect and wh-questions) in diverse samples of Mandarin-acquiring preschoolers with ASD, all utilizing the Intermodal Preferential Looking (IPL) paradigm. Results showed that children with ASD, though they were delayed in chronological age and expressive language (including significantly lower vocabulary production scores), acquired various grammatical constructions similarly to their typically developing peers. Moreover, Mandarin-acquiring preschoolers with ASD demonstrated similar acquisition patterns of these three core grammatical structures, as has been reported in previous IPL studies among English-acquiring children with ASD (Naigles &amp; Fein, 2017). Thus, the results testify that universal underlying mechanisms are playing vital roles in grammatical acquisition of children with ASD across languages (e.g., the setting of word order parameters, the preservation of functional morphemes, the universal operation of WH-Movement), despite their pervasive social cognition impairments. These findings suggest that core grammatical knowledge may be preserved in children with ASD, even in the face of radical differences in language environment and social/communicative deficits, supporting the contribution of the language faculty in autistic language acquisition. The results shed light on the sharp contrast between linguistic competence (governed by the internal computational system of the language faculty) vs. linguistic performance (affected by loci of impairment in the sensory-motor and the conceptual-intentional interfaces) in ASD. Furthermore, the results highlight the dissociation between the lexical vs. the grammatical modules in ASD, supporting a modular view of the diverse language domains in the language faculty.

The CaV1.2 G406R mutation decreases synaptic inhibition and alters L-type Ca2+ channel-dependent LTP at hippocampal synapses in a mouse model of Timothy Syndrome

Genetic alterations in autism spectrum disorders (ASD) frequently disrupt balance between synaptic excitation and inhibition and alter plasticity in the hippocampal CA1 region. Individuals with Timothy Syndrome (TS), a genetic disorder caused by CaV1.2 L-type Ca2+ channel (LTCC) gain-of function mutations, such as G406R, exhibit social deficits, repetitive behaviors, and cognitive impairments characteristic of ASD that are phenocopied in TS2-neo mice expressing G406R. Here, we characterized hippocampal CA1 synaptic function in male TS2-neo mice and found basal excitatory transmission was slightly increased and inhibitory transmission strongly decreased. We also found distinct impacts on two LTCC-dependent forms of long-term potentiation (LTP) synaptic plasticity that were not readily consistent with LTCC gain-of-function. LTP induced by high-frequency stimulation (HFS) was strongly impaired in TS2-neo mice, suggesting decreased LTCC function. Yet, CaV1.2 expression, basal phosphorylation, and current density were similar for WT and TS2-neo. However, this HFS-LTP also required GABAA receptor activity, and thus may be impaired in TS2-neo due to decreased inhibitory transmission. In contrast, LTP induced in WT mice by prolonged theta-train (PTT) stimulation in the presence of a β-adrenergic receptor agonist to increase CaV1.2 phosphorylation was partially induced in TS2-neo mice by PTT stimulation alone, consistent with increased LTCC function. Overall, our findings provide insights regarding how altered CaV1.2 channel function disrupts basal transmission and plasticity that could be relevant for neurobehavioral alterations in ASD.This article is part of the Special Issue on ‘L-type calcium channel mechanisms in neuropsychiatric disorders’.

Cognitive Impairment Associated with Schizophrenia: From Pathophysiology to Treatment.

Cognitive impairment is a core feature of schizophrenia and a major contributor to poor functional outcomes. Methods for assessment of cognitive dysfunction in schizophrenia are now well established. In addition, there has been increasing appreciation in recent years of the additional role of social cognitive impairment in driving functional outcomes and of the contributions of sensory-level dysfunction to higher-order impairments. At the neurochemical level, acute administration of N-methyl-d-aspartate receptor (NMDAR) antagonists reproduces the pattern of neurocognitive dysfunction associated with schizophrenia, encouraging the development of treatments targeted at both NMDAR and its interactome. At the local-circuit level, an auditory neurophysiological measure, mismatch negativity, has emerged both as a veridical index of NMDAR dysfunction and excitatory/inhibitory imbalance in schizophrenia and as a critical biomarker for early-stage translational drug development. Although no compounds have yet been approved for treatment of cognitive impairment associated with schizophrenia, several candidates are showing promise in early-phase testing.

Relapse of first-episode schizophrenia patients and neurocognitive impairment: The role of dopaminergic and anticholinergic burden

BackgroundThe prevention of relapse may be a key factor to diminish the cognitive impairment of first-episode schizophrenia (FES) patients. We aimed to ascertain the effects of relapse, and dopaminergic and anticholinergic treatment burdens on cognitive functioning in the follow-up. MethodsNinety-nine FES patients participated in this study. Cognitive assessments were performed at baseline and after 3 years of follow-up or, in those patients who relapsed, after >2 months of stabilization of the new acute psychotic episode. The primary outcomes were final cognitive dimensions. ResultsRepeated measures MANOVA analyses showed improvements in the whole sample on the end-point assessments in processing speed and social cognition. However, only impairment in social cognition showed a significant interaction with relapse by time in this sample.Relapse in FES patients was significantly associated with poor performance on end-point assessments of working memory, social cognition and global cognitive score. Anticholinergic burden, but not dopaminergic burden, was associated with verbal memory impairment. These significant associations resulted after controlling for baseline cognitive functioning, relapse and dopaminergic burden. ConclusionsThe relationship between relapse and cognitive impairment in recovered FES patients seems to be particularly complex at the short-term follow-up of these patients. While relapse was associated with working memory, social cognition impairments and global cognitive score, anticholinergic burden might play an additional worsening effect on verbal memory. Thus, tailoring or changing antipsychotics and other drugs to reduce their anticholinergic burden may be a potential modifiable factor to diminish cognitive impairment at this stage of the illness.

Reading the mind in the eyes in PTSD: Limited Moderation by the presence of a service dog

Persons with posttraumatic stress disorder (PTSD) frequently experience relationship failures in family and occupational domains resulting in loss of social supports. Prior research has implicated impairments in social cognition. The Reading the Mind in the Eyes Test (RMET) measures a key component of social cognition, the ability to infer the internal states of other persons based on features of the eyes region of the face; however, studies administering this popular test to persons with PTSD have yielded mixed results. This study assessed RMET performance in 47 male U.S. military Veterans with chronic, severe PTSD. Employing a within-subjects design that avoided selection biases, it aimed specifically to determine whether components of RMET performance, including accuracy, response latency, and stimulus dwell time, were improved by the company of a service dog, an intervention that has improved social function in other populations. RMET accuracies and response latencies in this PTSD sample were in the normal range. The presence of a familiar service dog did not improve RMET accuracy, reduce response latencies, or increase dwell times. Dog presence increased the speed of visual scanning perhaps consistent with reduced social fear.

Relationship between the domains of theory of mind, social dysfunction, and oxytocin in schizophrenia

Social dysfunction, manifested by impaired social cognition, is contributing to poorer prognosis of patients with schizophrenia. Growing evidence indicates that oxytocin acts as a neurotransmitter in the regulation of social cognition. It still lacks a thorough understanding of how oxytocin is linked with deficits in social cognition and social functioning in schizophrenia. To this end, we aimed to study the role of plasma oxytocin levels in the relationship between subdomains of social cognition and social dysfunction in patients with schizophrenia. Social Functioning Scale was administered to measure social dysfunction while Faux Pas Recognition Test was used to assess the Theory of Mind (ToM) in 40 patients with schizophrenia and 40 age-matched healthy controls. Patients with schizophrenia exhibited more deficits in ToM, more severe social dysfunction, and had lower plasma oxytocin levels, relative to healthy controls. A pooled correlation analysis of all participants revealed significant effects of plasma oxytocin levels on the ToM and social dysfunction. In patients with schizophrenia, plasma oxytocin levels were positively correlated with the affective but not cognitive component of the ToM, and the effects of plasma oxytocin levels on social functioning were partially mediated by affective ToM. Our findings underscore the importance of oxytocin as a potential predictor of ToM and social functioning in patients with schizophrenia. It may be worthwhile for future studies of oxytocin in schizophrenia to focus on an affected behavioral domain, e.g., social cognition, rather than diagnosis, and the targeted domain should be deconstructed into more detailed subdomains.

Oxytocin in Huntington's disease and the spectrum of amyotrophic lateral sclerosis-frontotemporal dementia.

Neurodegenerative disorders (NDDs) such as Huntington’s disease (HD) and the spectrum of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are characterized by progressive loss of selectively vulnerable populations of neurons. Although often associated with motor impairments, these NDDs share several commonalities in early symptoms and signs that extend beyond motor dysfunction. These include impairments in social cognition and psychiatric symptoms. Oxytocin (OXT) is a neuropeptide known to play a pivotal role in the regulation of social cognition as well as in emotional behaviors such as anxiety and depression. Here, we present an overview of key results implicating OXT in the pathology of HD, ALS and FTD and seek to identify commonalities across these NDDs. OXT is produced in the hypothalamus, a region in the brain that during the past decade has been shown to be affected in HD, ALS, and FTD. Several studies using human post-mortem neuropathological analyses, measurements of cerebrospinal fluid, experimental treatments with OXT as well as genetic animal models have collectively implicated an important role of central OXT in the development of altered social cognition and psychiatric features across these diseases. Understanding central OXT signaling may unveil the underlying mechanisms of early signs of the social cognitive impairment and the psychiatric features in NDDs. It is therefore possible that OXT might have potential therapeutic value for early disease intervention and better symptomatic treatment in NDDs.

Corpus Callosum Microstructural Tract Integrity Relates to Longer Emotion Recognition Reaction Time in People with Schizophrenia.

Objective: Schizophrenia is a complex functionally debilitating neurodevelopmental disorder, with associated social cognitive impairment. Corpus Callosum (CC) white matter tracts deficits are reported for people with schizophrenia; however, few studies focus on interhemispheric processing relative to social cognition tasks. This study aimed to determine if a relationship between the CC and social cognition exists. Method: In this cross-section study, a sample of n = 178 typical controls and n = 58 people with schizophrenia completed measures of mentalising (Reading the Mind in the Eyes), emotion recognition outcome and reaction time (Emotion Recognition Test), and clinical symptoms (Positive and Negative Symptom Scale), alongside diffusion-based tract imaging. The CC and its subregions, i.e., the genu, body, and splenium were the regions of interest (ROI). Results: Reduced white matter tract integrity was observed in the CC for patients when compared to controls. Patients performed slower, and less accurately on emotion recognition tasks, which significantly and negatively correlated to the structural integrity of the CC genu. Tract integrity further significantly and negatively related to clinical symptomatology. Conclusions: People with schizophrenia have altered white matter integrity in the genu of the CC, compared to controls, which relates to cognitive deficits associated with recognising emotional stimuli accurately and quickly, and severity of clinical symptoms.