The impact of negative mood state on sleep-related attentional bias in insomnia.
Zheng Senning,Feng Juan,Lin Rongmao,Yan Youwei,Zhang Renchuan,Huang Huiyuan,Wang Junjing,Huang Ruiwang
Journal of sleep research
Sleep-related attentional bias is thought to play a role in the maintenance of insomnia. However, this concept has been questioned by several studies that did not show the presence of sleep-related attentional bias in clinical insomnia or poor sleepers. Our goal in the present study was to test whether the mood state of individuals with insomnia affects the presence of sleep-related attentional bias. To this end, 31 individuals with insomnia and 34 good sleepers were randomly assigned to a negative mood-inducing condition or a control condition. They then completed a visual probe task with three types of pictorial stimuli (general threat, sleep-related negative pictures and sleep-related positive pictures). Vigilance, maintenance and the overall bias indexes were calculated based on the reaction time. We found individuals with insomnia only showed a greater overall bias compared with good sleepers following a negative mood induction, regardless of the pictures presented. In addition, we found that a negative mood state was significantly correlated with the overall attentional bias in good sleepers but not in individuals with insomnia. These findings suggest that sleep-related attentional bias in insomnia can be modulated by mood state. This effect may reflect the dysregulation of top-down attentional control in individuals with insomnia.
10.1111/jsr.12748
Meta-analysis of functional neuroimaging studies of emotion perception and experience in schizophrenia.
Taylor Stephan F,Kang Jian,Brege Inga S,Tso Ivy F,Hosanagar Avinash,Johnson Timothy D
Biological psychiatry
BACKGROUND:Neuroimaging studies of emotion in schizophrenia have reported abnormalities in amygdala and other regions, although divergent results and heterogeneous paradigms complicate conclusions from single experiments. To identify more consistent patterns of dysfunction, a meta-analysis of functional imaging studies of emotion was undertaken. METHODS:Searching Medline and PsycINFO databases through January 2011, 88 potential articles were identified, of which 26 met inclusion criteria, comprising 450 patients with schizophrenia and 422 healthy comparison subjects. Contrasts were selected to include emotion perception and emotion experience. Foci from individual studies were subjected to a voxelwise meta-analysis using multilevel kernel density analysis. RESULTS:For emotional experience, comparison subjects showed greater activation in the left occipital pole. For emotional perception, schizophrenia subjects showed reduced activation in bilateral amygdala, visual processing areas, anterior cingulate cortex, dorsolateral frontal cortex, medial frontal cortex, and subcortical structures. Schizophrenia subjects showed greater activation in the cuneus, parietal lobule, precentral gyrus, and superior temporal gyrus. Combining across studies and eliminating studies that did not balance on effort and stimulus complexity eliminated most differences in visual processing regions as well as most areas where schizophrenia subjects showed a greater signal. Reduced reactivity of the amygdala appeared primarily in implicit studies of emotion, whereas deficits in anterior cingulate cortex activity appeared throughout all contrasts. CONCLUSIONS:Processing emotional stimuli, schizophrenia patients show reduced activation in areas engaged by emotional stimuli, although in some conditions, schizophrenia patients exhibit increased activation in areas outside those traditionally associated with emotion, possibly representing compensatory processing.
10.1016/j.biopsych.2011.09.007
Adjunctive raloxifene treatment improves attention and memory in men and women with schizophrenia.
Weickert T W,Weinberg D,Lenroot R,Catts S V,Wells R,Vercammen A,O'Donnell M,Galletly C,Liu D,Balzan R,Short B,Pellen D,Curtis J,Carr V J,Kulkarni J,Schofield P R,Weickert C S
Molecular psychiatry
There is increasing clinical and molecular evidence for the role of hormones and specifically estrogen and its receptor in schizophrenia. A selective estrogen receptor modulator, raloxifene, stimulates estrogen-like activity in brain and can improve cognition in older adults. The present study tested the extent to which adjunctive raloxifene treatment improved cognition and reduced symptoms in young to middle-age men and women with schizophrenia. Ninety-eight patients with a diagnosis of schizophrenia or schizoaffective disorder were recruited into a dual-site, thirteen-week, randomized, double-blind, placebo-controlled, crossover trial of adjunctive raloxifene treatment in addition to their usual antipsychotic medications. Symptom severity and cognition in the domains of working memory, attention/processing speed, language and verbal memory were assessed at baseline, 6 and 13 weeks. Analyses of the initial 6-week phase of the study using a parallel groups design (with 39 patients receiving placebo and 40 receiving raloxifene) revealed that participants receiving adjunctive raloxifene treatment showed significant improvement relative to placebo in memory and attention/processing speed. There was no reduction in symptom severity with treatment compared with placebo. There were significant carryover effects, suggesting some cognitive benefits are sustained even after raloxifene withdrawal. Analysis of the 13-week crossover data revealed significant improvement with raloxifene only in attention/processing speed. This is the first study to show that daily, oral adjunctive raloxifene treatment at 120 mg per day has beneficial effects on attention/processing speed and memory for both men and women with schizophrenia. Thus, raloxifene may be useful as an adjunctive treatment for cognitive deficits associated with schizophrenia.
10.1038/mp.2015.11
Prefrontal activation deficits during episodic memory in schizophrenia.
Ragland John D,Laird Angela R,Ranganath Charan,Blumenfeld Robert S,Gonzales Sabina M,Glahn David C
The American journal of psychiatry
OBJECTIVE:Episodic memory impairments represent a core deficit in schizophrenia that severely limits patients' functional outcome. This quantitative meta-analysis of functional imaging studies of episodic encoding and retrieval tests the prediction that these deficits are most consistently associated with dysfunction in the prefrontal cortex. METHOD:Activation likelihood estimation (ALE) was used to perform a quantitative meta-analysis of functional imaging studies that contrasted patients with schizophrenia and healthy volunteers during episodic encoding and retrieval. From a pool of 36 potential studies, 18 whole-brain studies in standard space that included a healthy comparison sample and low-level baseline contrast were selected. RESULTS:As predicted, patients showed less prefrontal activation than comparison subjects in the frontal pole, dorsolateral and ventrolateral prefrontal cortex during encoding, and the dorsolateral prefrontal cortex and ventrolateral prefrontal cortex during retrieval. The ventrolateral prefrontal cortex encoding deficits were not present in studies that provided patients with encoding strategies, but dorsolateral prefrontal cortex deficits remained and were not secondary to group performance differences. The only medial temporal lobe finding was relatively greater patient versus comparison subject activation in the parahippocampal gyrus during encoding and retrieval. CONCLUSIONS:The finding of prominent prefrontal dysfunction suggests that cognitive control deficits strongly contribute to episodic memory impairment in schizophrenia. Memory rehabilitation approaches developed for patients with frontal lobe lesions and pharmacotherapy approaches designed to improve prefrontal cortex function may therefore hold special promise for remediating memory deficits in patients with schizophrenia.
10.1176/appi.ajp.2009.08091307
Processing speed deficits in schizophrenia: reexamining the evidence.
Knowles Emma E M,David Anthony S,Reichenberg Abraham
The American journal of psychiatry
OBJECTIVE:A recent meta-analysis identified processing speed inefficiency as the largest single cognitive impairment in schizophrenia. However, the effect of potential moderator variables, such as medication status and severity of illness, remained unclear. The authors present an extended meta-analysis of processing speed and other specific cognitive functions in schizophrenia and examine the role of potential moderator variables. METHOD:In addition to the studies identified in the original analysis, subsequently published articles were identified via systematic searches of MEDLINE and PsycINFO for the period from May 2006 to January 2009. The authors extracted data for potential moderator variables, including publication year; severity of illness; chlorpromazine equivalent daily dose; and mean IQ, mean age, and sample size for each study. Effect sizes were calculated for all measures, and meta-influence and homogeneity analyses were conducted. RESULTS:Eleven studies were added to the original analysis, increasing the schizophrenia sample size from 1,915 to 4,135. The largest effect size was for coding tasks (g=-1.50), followed by category fluency (g=-1.31). However, for coding tasks, variation in effect size magnitude attributable to heterogeneity was substantial. Metaregression analyses indicated that three moderator variables were related to coding task effect size: publication year, IQ difference from comparison subjects, and chlorpromazine equivalent daily dose. There was a difference of 0.8 effect size units between studies with low compared with high chlorpromazine equivalent daily dose. No significant relationships were found between any moderators and the other cognitive tasks included in the meta-analysis. CONCLUSIONS:The processing speed impairment in schizophrenia is substantially affected by several moderating factors, in particular antipsychotic medication dosage.
10.1176/appi.ajp.2010.09070937
Social cognition in schizophrenia.
Green Michael F,Horan William P,Lee Junghee
Nature reviews. Neuroscience
Individuals with schizophrenia exhibit impaired social cognition, which manifests as difficulties in identifying emotions, feeing connected to others, inferring people's thoughts and reacting emotionally to others. These social cognitive impairments interfere with social connections and are strong determinants of the degree of impaired daily functioning in such individuals. Here, we review recent findings from the fields of social cognition and social neuroscience and identify the social processes that are impaired in schizophrenia. We also consider empathy as an example of a complex social cognitive function that integrates several social processes and is impaired in schizophrenia. This information may guide interventions to improve social cognition in patients with this disorder.
10.1038/nrn4005
Cognition in schizophrenia: core psychological and neural mechanisms.
Barch Deanna M,Ceaser Alan
Trends in cognitive sciences
The challenge in understanding cognitive impairment in schizophrenia is that people with this illness have deficits in an array of domains. Here, we briefly review evidence regarding the pattern of deficits within three domains: context processing, working memory and episodic memory. We suggest that there may be a common mechanism driving deficits in these domains - an impairment in the ability to actively represent goal information in working memory to guide behavior, a function we refer to as proactive control. We suggest that such deficits in proactive control reflect impairments in dorsolateral prefrontal cortex, its interactions with other brain regions, such as parietal cortex, thalamus and striatum, and the influence of neurotransmitter systems, such as dopamine, GABA and glutamate.
10.1016/j.tics.2011.11.015
Identification of Genetic Loci Jointly Influencing Schizophrenia Risk and the Cognitive Traits of Verbal-Numerical Reasoning, Reaction Time, and General Cognitive Function.
Smeland Olav B,Frei Oleksandr,Kauppi Karolina,Hill W David,Li Wen,Wang Yunpeng,Krull Florian,Bettella Francesco,Eriksen Jon A,Witoelar Aree,Davies Gail,Fan Chun C,Thompson Wesley K,Lam Max,Lencz Todd,Chen Chi-Hua,Ueland Torill,Jönsson Erik G,Djurovic Srdjan,Deary Ian J,Dale Anders M,Andreassen Ole A,
JAMA psychiatry
Importance:Schizophrenia is associated with widespread cognitive impairments. Although cognitive deficits are one of the factors most strongly associated with functional outcome in schizophrenia, current treatment strategies largely fail to ameliorate these impairments. To develop more efficient treatment strategies in patients with schizophrenia, a better understanding of the pathogenesis of these cognitive deficits is needed. Accumulating evidence indicates that genetic risk of schizophrenia may contribute to cognitive dysfunction. Objective:To identify genomic regions jointly influencing schizophrenia and the cognitive domains of reaction time and verbal-numerical reasoning, as well as general cognitive function, a phenotype that captures the shared variation in performance across cognitive domains. Design, Setting, and Participants:Combining data from genome-wide association studies from multiple phenotypes using conditional false discovery rate analysis provides increased power to discover genetic variants and could elucidate shared molecular genetic mechanisms. Data from the following genome-wide association studies, published from July 24, 2014, to January 17, 2017, were combined: schizophrenia in the Psychiatric Genomics Consortium cohort (n = 79 757 [cases, 34 486; controls, 45 271]); verbal-numerical reasoning (n = 36 035) and reaction time (n = 111 483) in the UK Biobank cohort; and general cognitive function in CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) (n = 53 949) and COGENT (Cognitive Genomics Consortium) (n = 27 888). Main Outcomes and Measures:Genetic loci identified by conditional false discovery rate analysis. Brain messenger RNA expression and brain expression quantitative trait locus functionality were determined. Results:Among the participants in the genome-wide association studies, 21 loci jointly influencing schizophrenia and cognitive traits were identified: 2 loci shared between schizophrenia and verbal-numerical reasoning, 6 loci shared between schizophrenia and reaction time, and 14 loci shared between schizophrenia and general cognitive function. One locus was shared between schizophrenia and 2 cognitive traits and represented the strongest shared signal detected (nearest gene TCF20; chromosome 22q13.2), and was shared between schizophrenia (z score, 5.01; P = 5.53 × 10-7), general cognitive function (z score, -4.43; P = 9.42 × 10-6), and verbal-numerical reasoning (z score, -5.43; P = 5.64 × 10-8). For 18 loci, schizophrenia risk alleles were associated with poorer cognitive performance. The implicated genes are expressed in the developmental and adult human brain. Replicable expression quantitative trait locus functionality was identified for 4 loci in the adult human brain. Conclusions and Relevance:The discovered loci improve the understanding of the common genetic basis underlying schizophrenia and cognitive function, suggesting novel molecular genetic mechanisms.
10.1001/jamapsychiatry.2017.1986
Polygenic disruption of retinoid signalling in schizophrenia and a severe cognitive deficit subtype.
Molecular psychiatry
Retinoid metabolites of vitamin A are intrinsically linked to neural development, connectivity and plasticity, and have been implicated in the pathophysiology of schizophrenia. We hypothesised that a greater burden of common and rare genomic variation in genes involved with retinoid biogenesis and signalling could be associated with schizophrenia and its cognitive symptoms. Common variants associated with schizophrenia in the largest genome-wide association study were aggregated in retinoid genes and used to formulate a polygenic risk score (PRS) for each participant in the Australian Schizophrenia Research Bank. In support of our hypothesis, we found PRS to be significantly associated with the disorder. Cases with severe cognitive deficits, while not further differentiated by PRS, were enriched with rare variation in the retinoic acid receptor beta gene RARB, detected through whole-genome sequencing. RARB rare variant burden was also associated with reduced cerebellar volume in the cases with marked cognitive deficit, and with covariation in grey matter throughout the brain. An excess of rare variation was further observed in schizophrenia in retinoic acid response elements proximal to target genes, which we show are differentially expressed in the disorder in two RNA sequencing datasets. Our results suggest that genomic variation may disrupt retinoid signalling in schizophrenia, with particular significance for cases with severe cognitive impairment.
10.1038/s41380-018-0305-0
Memory and cognition in schizophrenia.
Molecular psychiatry
Episodic memory deficits are consistently documented as a core aspect of cognitive dysfunction in schizophrenia patients, present from the onset of the illness and strongly associated with functional disability. Over the past decade, research using approaches from experimental cognitive neuroscience revealed disproportionate episodic memory impairments in schizophrenia (Sz) under high cognitive demand relational encoding conditions and relatively unimpaired performance under item-specific encoding conditions. These specific deficits in component processes of episodic memory reflect impaired activation and connectivity within specific elements of frontal-medial temporal lobe circuits, with a central role for the dorsolateral prefrontal cortex (DLPFC), relatively intact function of ventrolateral prefrontal cortex and variable results in the hippocampus. We propose that memory deficits can be understood within the broader context of cognitive deficits in Sz, where impaired DLPFC-related cognitive control has a broad impact across multiple cognitive domains. The therapeutic implications of these findings are discussed.
10.1038/s41380-018-0231-1
Evidence of Common Genetic Overlap Between Schizophrenia and Cognition.
Hubbard Leon,Tansey Katherine E,Rai Dheeraj,Jones Peter,Ripke Stephan,Chambert Kimberly D,Moran Jennifer L,McCarroll Steven A,Linden David E J,Owen Michael J,O'Donovan Michael C,Walters James T R,Zammit Stanley
Schizophrenia bulletin
Cognitive impairment is a core feature of schizophrenia but there is limited understanding of the genetic relationship between cognition in the general population and schizophrenia. We examine how common variants associated with schizophreniaen massecontribute to childhood cognitive ability in a population-based sample, and the extent to which common genetic variants associated with childhood cognition explain variation in schizophrenia. Schizophrenia polygenic risk scores were derived from the Psychiatric Genomics Consortium (n= 69 516) and tested for association with IQ, attention, processing speed, working memory, problem solving, and social cognition in over 5000 children aged 8 from the Avon Longitudinal Study of Parents and Children birth cohort. Polygenic scores for these cognitive domains were tested for association with schizophrenia in a large UK schizophrenia sample (n= 11 853). Bivariate genome-wide complex trait analysis (GCTA) estimated the amount of shared genetic factors between schizophrenia and cognitive domains. Schizophrenia polygenic risk score was associated with lower performance IQ (P= .001) and lower full IQ (P= .013). Polygenic score for performance IQ was associated with increased risk for schizophrenia (P= 3.56E-04). Bivariate GCTA revealed moderate genetic correlation between schizophrenia and both performance IQ (rG= -.379,P= 6.62E-05) and full IQ (rG= -.202,P= 5.00E-03), with approximately 14% of the genetic component of schizophrenia shared with that for performance IQ. Our results support the presence of shared common genetic factors between schizophrenia and childhood cognitive ability. We observe a genetic relationship between schizophrenia and performance IQ but not verbal IQ or other cognitive variables, which may have implications for studies utilizing cognitive endophenotypes for psychosis.
10.1093/schbul/sbv168
Associations between P3a and P3b amplitudes and cognition in antipsychotic-naïve first-episode schizophrenia patients.
Kruiper Caitlyn,Fagerlund Birgitte,Nielsen Mette Ø,Düring Signe,Jensen Maria H,Ebdrup Bjørn H,Glenthøj Birte Y,Oranje Bob
Psychological medicine
BACKGROUND:Cognitive deficits are already present in early stages of schizophrenia. P3a and P3b event-related potentials (ERPs) are believed to underlie the processes of attention and working memory (WM), yet limited research has been performed on the associations between these parameters. Therefore, we explored possible associations between P3a/b amplitudes and cognition in a large cohort of antipsychotic-naïve, first-episode schizophrenia (AN-FES) patients and healthy controls (HC). METHODS:Seventy-three AN-FES patients and 93 age- and gender-matched HC were assessed for their P3a/b amplitude with an auditory oddball paradigm. In addition, subjects performed several subtests from the Cambridge Neuropsychological Test Automated Battery (CANTAB). RESULTS:AN-FES patients had significantly reduced P3a/b amplitudes, as well as significantly lower scores on all cognitive tests compared with HC. Total group correlations revealed positive associations between P3b amplitude and WM and sustained attention and negative associations with all reaction time measures. These associations appeared mainly driven by AN-FES patients, where we found a similar pattern. No significant associations were found between P3b amplitude and cognitive measures in our HC. P3a amplitude did not correlate significantly with any cognitive measures in either group, nor when combined. CONCLUSIONS:Our results provide further evidence for P3a/b amplitude deficits and cognitive deficits in AN-FES patients, which are neither due to antipsychotics nor to disease progress. Furthermore, our data showed significant, yet weak associations between P3b and cognition. Therefore, our data do not supply evidence for deficient P3a/b amplitudes as direct underlying factors for cognitive deficits in schizophrenia.
10.1017/S0033291718001575
A Schizophrenia-Related Genetic-Brain-Cognition Pathway Revealed in a Large Chinese Population.
EBioMedicine
BACKGROUND:In the past decades, substantial effort has been made to explore the genetic influence on brain structural/functional abnormalities in schizophrenia, as well as cognitive impairments. In this work, we aimed to extend previous studies to explore the internal mediation pathway among genetic factor, brain features and cognitive scores in a large Chinese dataset. METHODS:Gray matter (GM) volume, fractional amplitude of low-frequency fluctuations (fALFF), and 4522 schizophrenia-susceptible single nucleotide polymorphisms (SNP) from 905 Chinese subjects were jointly analyzed, to investigate the multimodal association. Based on the identified imaging-genetic pattern, correlations with cognition and mediation analysis were then conducted to reveal the potential mediation pathways. FINDINGS:One linked imaging-genetic pattern was identified to be group discriminative, which was also associated with working memory performance. Particularly, GM reduction in thalamus, putamen and bilateral temporal gyrus in schizophrenia was associated with fALFF decrease in medial prefrontal cortex, both were also associated with genetic factors enriched in neuron development, synapse organization and axon pathways, highlighting genes including CSMD1, CNTNAP2, DCC, GABBR2 etc. This linked pattern was also replicated in an independent cohort (166 subjects), which although showed certain age and clinical differences with the discovery cohort. A further mediation analysis suggested that GM alterations significantly mediated the association from SNP to fALFF, while fALFF mediated the association from SNP and GM to working memory performance. INTERPRETATION:This study has not only verified the impaired imaging-genetic association in schizophrenia, but also initially revealed a potential genetic-brain-cognition mediation pathway, indicating that polygenic risk factors could exert impact on phenotypic measures from brain structure to function, thus could further affect cognition in schizophrenia.
10.1016/j.ebiom.2018.10.009
Cognition and Reward Circuits in Schizophrenia: Synergistic, Not Separate.
Robison A J,Thakkar Katharine N,Diwadkar Vaibhav A
Biological psychiatry
Schizophrenia has been studied from the perspective of cognitive or reward-related impairments, yet it cannot be wholly related to one or the other process and their corresponding neural circuits. We posit a comprehensive circuit-based model proposing that dysfunctional interactions between the brain's cognitive and reward circuits underlie schizophrenia. The model is underpinned by how the relationship between glutamatergic and dopaminergic dysfunction in schizophrenia drives interactions between cognition and reward circuits. We argue that this interaction is synergistic: that is, deficits of cognition and reward processing interact, and this interaction is a core feature of schizophrenia. In adopting this position, we undertake a focused review of animal physiology and human clinical data, and in proposing this synergistic model, we highlight dopaminergic afferents from the ventral tegmental area to nucleus accumbens (mesolimbic circuit) and frontal cortex (mesocortical circuit). We then expand on the role of glutamatergic inputs to these dopamine circuits and dopaminergic modulation of critical excitatory pathways with attention given to the role of glutamatergic hippocampal outputs onto nucleus accumbens. Finally, we present evidence for how in schizophrenia, dysfunction in the mesolimbic and mesocortical circuits and their corresponding glutamatergic inputs gives rise to clinical and cognitive phenotypes and is associated with positive and negative symptom dimensions. The synthesis attempted here provides an impetus for a conceptual shift that links cognitive and motivational aspects of schizophrenia and that can lead to treatment approaches that seek to harmonize network interactions between the brain's cognition and reward circuits with ameliorative effects in each behavioral domain.
10.1016/j.biopsych.2019.09.021
Linking resting-state networks and social cognition in schizophrenia and bipolar disorder.
Jimenez Amy M,Riedel Philipp,Lee Junghee,Reavis Eric A,Green Michael F
Human brain mapping
Individuals with schizophrenia and bipolar disorder show alterations in functional neural connectivity during rest. However, resting-state network (RSN) disruptions have not been systematically compared between the two disorders. Further, the impact of RSN disruptions on social cognition, a key determinant of functional outcome, has not been studied. Forty-eight individuals with schizophrenia, 46 with bipolar disorder, and 48 healthy controls completed resting-state functional magnetic resonance imaging. An atlas-based approach was used to examine functional connectivity within nine RSNs across the cortex. RSN connectivity was assessed via nonparametric permutation testing, and associations with performance on emotion perception, mentalizing, and emotion management tasks were examined. Group differences were observed in the medial and lateral visual networks and the sensorimotor network. Individuals with schizophrenia demonstrated reduced connectivity relative to healthy controls in all three networks. Individuals with bipolar disorder demonstrated reduced connectivity relative to controls in the medial visual network and connectivity within this network was significantly positively correlated with emotion management. In healthy controls, connectivity within the medial and lateral visual networks positively correlated with mentalizing. No significant correlations were found for either visual network in schizophrenia. Results highlight the role of altered early visual processing in social cognitive deficits in both schizophrenia and bipolar disorder. However, individuals with bipolar disorder appear to compensate for disrupted visual network connectivity on social cognitive tasks, whereas those with schizophrenia do not. The current study adds clarity on the neurophysiology underlying social cognitive deficits that result in impaired functioning in serious mental illness.
10.1002/hbm.24731
Neurobiology and treatment of social cognition in schizophrenia: Bridging the bed-bench gap.
Kimoto Sohei,Makinodan Manabu,Kishimoto Toshifumi
Neurobiology of disease
Social cognition refers to the psychological processes involved in the perception, encoding, storage, retrieval, and regulation of information about others and ourselves. This process is essential for survival and reproduction in complex social environments. Recent evidence suggests that impairments in social cognition frequently occur in schizophrenia, mainly contributing to poor functional outcomes, including the inability to engage in meaningful work and maintain satisfying interpersonal relationships. With the ambiguous definition of social cognition, the neurobiology underlying impaired social cognition remains unknown, and the effectiveness of currently available intervention strategies in schizophrenia remain limited. Considering the advances and challenges of translational research for schizophrenia, social cognition has been considered a high-priority domain for treatment development. Here, we describe the current state of the framework, clinical concerns, and intervention approaches for social cognition in schizophrenia. Next, we introduce translatable rodent models associated with schizophrenia that allow the evaluation of different components of social behaviors, providing deeper insights into the neural substrates of social cognition in schizophrenia. Our review presents a valuable perspective that indicates the necessity of building bridges between basic and clinical science researchers for the development of novel therapeutic approaches in impaired social cognition in schizophrenia.
10.1016/j.nbd.2018.10.022