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Abstract Background Schizophrenia (SCZ) and treatment-resistant schizophrenia (TRS) are associated with aberrations in immune-inflammatory pathways. Increased high mobility group protein 1 (HMGB1), an inflammatory mediator, and Dickkopf-related protein (DKK1), a Wnt/β-catenin signaling antagonist, affect the blood-brain barrier and induce neurotoxic effects and neurocognitive deficits. Aim The present study aims to examine HMGB1 and DDK1 in nonresponders to treatments (NRTT) with antipsychotics (n = 60), partial RTT (PRTT, n = 55), and healthy controls (n = 43) in relation to established markers of SCZ, including interleukin (IL)-6, IL-10, and CCL11 (eotaxin), and to delineate whether these proteins are associated with the SCZ symptom subdomains and neurocognitive impairments. Results HMGB1, DKK1, IL-6, and CCL11 were significantly higher in SCZ patients than in controls. DKK1 and IL-6 were significantly higher in NRTT than in PRTT and controls, while IL-10 was higher in NRTT than in controls. Binary logistic regression analysis showed that SCZ was best predicted by increased DDK1 and HMGB1, while NRTT (vs PRTT) was best predicted by increased IL-6 and CCL11 levels. A large part of the variance in psychosis, hostility, excitation, mannerism, and negative (PHEMN) symptoms and formal thought disorders was explained by HMGB1, IL-6, and CCL11, while most neurocognitive functions were predicted by HMGB1, DDK1, and CCL11. Conclusions The neurotoxic effects of HMGB1, DKK1, IL-6, and CCL11 including the effects on the blood-brain barrier and the Wnt/β-catenin signaling pathway may cause impairments in executive functions and working, episodic, and semantic memory and explain, in part, PHEMN symptoms and a nonresponse to treatment with antipsychotic drugs.

It is well established that poor inhibitory control confers both a vulnerability to, and maintenance of, addictive behaviors across the substance and behavioral spectrums. By comparison, the role of compulsivity in addictive behaviors has received less research focus. The neurocognitive literature to date is vast, and it is unclear whether there are any convincing lines of systematic evidence delineating whether and how aspects of impulsivity and compulsivity are shared and unique across different substance and behavioral addictive disorders. Such information has significant implications for our understanding of underlying mechanisms and clinical implications for assessing and treating neurocognitive deficits across addictions. Here, we conducted a systematic meta-review of the quantitative meta-analyses to date, specifically examining the neurocognitive functions central to impulsive-compulsive behaviors transdiagnostically across addictive behaviors. Out of 1186 empirical studies initially identified, six meta-analyses met inclusion criteria examining alcohol, cannabis, cocaine, MDMA, methamphetamine, opioid and tobacco use, as well as gambling and internet addiction. The pooled findings across the systematic meta-analyses suggest that impulsivity is a core process underpinning both substance and behavioral addictive disorders, although it is not equally implicated across all substances. Compulsivity-related neurocognition, by comparison, is important across alcohol and gambling disorders, but has yet to be examined systematically. The gestalt of findings to date suggests that both impulsivity and compulsivity are core constructs linked to addictive behaviors and may not be solely the secondary sequelae associated with the effects of prolonged substance exposure.

The relationship between cognition and the ability to hear is well known. Due to changes in demographics, the number of people with sensorineural hearing loss and cognitive impairment is increasing. The aim of this study was to identify the impact of hearing rehabilitation via cochlear implantation on cognitive decline among the aging population. This prospective study included 60 subjects aged between 50 and 84 years (mean 65.8 years, SD=8.9) with a severe to profound bilateral hearing impairment. A computer-based evaluation of short- and long-term memory, processing speed, attention, working memory and inhibition was performed prior to surgery as well as 6 and 12 months after cochlear implantation. Additionally, speech perception at 65 and 80 dB (Freiburger monosyllabic speech test) as well as disease-related (Nijmegen Cochlear Implant Questionnaire) and general (WHOQOL-OLD) quality of life were assessed. Six months postimplantation, speech perception, quality of life and also neurocognitive abilities significantly increased. The most remarkable improvement after 6 months was detected in executive functions such as attention ( <0.001), inhibition ( =0.025) and working memory (n-back: =0.002; operation span task: =0.008), followed by delayed recall ( =0.03). In contrast, long-term memory showed a significant change of performance only after 12 months ( =0.021). After 6 months, most cognitive domains remained stable, except working memory assessed by the operation span task, which significantly improved between 6 and 12 months ( <0.001). No correlation was found between cognitive results and duration of deafness, speech perception or quality of life. Cochlear implantation does not only lead to better speech perception and quality of life, but has also been shown to improve cognitive skills in hearing impaired adults aged 50 years or more. These effects seem to be independent of each other.

Autism spectrum disorder (ASD) and schizophrenia (SCZ) are separate neurodevelopmental disorders that are both characterized by difficulties in social cognition and social functioning. Due to methodological confounds, the degree of similarity in social cognitive impairments across these two disorders is currently unknown. This study therefore conducted a comprehensive comparison of social cognitive ability in ASD and SCZ to aid efforts to develop optimized treatment programs. In total, 101 individuals with ASD, 92 individuals with SCZ or schizoaffective disorder, and 101 typically developing (TD) controls, all with measured intelligence in the normal range and a mean age of 25.47 years, completed a large battery of psychometrically validated social cognitive assessments spanning the domains of emotion recognition, social perception, mental state attribution, and attributional style. Both ASD and SCZ performed worse than TD controls, and very few differences were evident between the two clinical groups, with effect sizes (Cohen's d) ranging from 0.01 to 0.34. For those effects that did reach statistical significance, such as greater hostility in the SCZ group, controlling for symptom severity rendered them non-significant, suggesting that clinical distinctions may underlie these social cognitive differences. Additionally, the strength of the relationship between neurocognitive and social cognitive performance was of similar, moderate size for ASD and SCZ. Findings largely suggest comparable levels of social cognitive impairment in ASD and SCZ, which may support the use of existing social cognitive interventions across disorders. However, future work is needed to determine whether the mechanisms underlying these shared impairments are also similar or if these common behavioral profiles may emerge via different pathways.

Positive attitude is thought to impact academic achievement and learning in children, but little is known about its underlying neurocognitive mechanisms. Using a large behavioral sample of 240 children, we found that positive attitude toward math uniquely predicted math achievement, even after we accounted for multiple other cognitive-affective factors. We then investigated the neural mechanisms underlying the link between positive attitude and academic achievement in two independent cohorts of children (discovery cohort: n = 47; replication cohort: n = 28) and tested competing hypotheses regarding the differential roles of affective-motivational and learning-memory systems. In both cohorts, we found that positive attitude was associated with increased engagement of the hippocampal learning-memory system. Structural equation modeling further revealed that, in both cohorts, increased hippocampal activity and more frequent use of efficient memory-based strategies mediated the relation between positive attitude and higher math achievement. Our study is the first to elucidate the neurocognitive mechanisms by which positive attitude influences learning and academic achievement.

Background Mixed dementia is characterized by significant clinical and pathological heterogeneity posing challenges for accurate diagnosis and treatment planning. Digital twin technology offers a transformative approach by learning data characteristics to simulate predictions of an unseen data sample. This study aims to construct a digital twin neural marker with multimodal neuroimage data to enable predictive tasks on samples with mixed dementia. We leverage cross‐site neuroimage datasets from the Dementias Platform UK (DPUK) and a Korean dementia cohort to construct the digital twin neural marker and show that the marker can be applied to delineate etiologies of mixed dementia. Methods A digital twin neural marker of mixed dementia was constructed by training a Vision Transformer (ViT) model with a generative pre‐training approach. Specifically, Masked AutoEncoder (MAE) training of the ViT model on T1w and FLAIR neuroimage data from DPUK and a Korean dementia cohort was first constructed to capture the latent characteristics of the neurodegenerative brain etiologies. The model was further fine‐tuned on another Korean dementia cohort data with mixed dementia to delineate the etiologies of the neurocognitive disorder given a neuroimage input. Federated learning approaches were employed to train the model without data transfer across sites, maintaining data privacy within the trusted research environment. Results The fine‐tuned digital twin neural marker achieved a reliable performance in delineating the mixed dementia etiology. The latent representation of the neural marker showed a separable pattern between different underlying etiologies when visualized with UMAP. These findings demonstrate the effectiveness of digital twins in leveraging global cross‐site datasets to provide actionable clinical insights. Conclusions The results highlight the potential of a digital twin neural marker to address the complexities of delineating mixed dementia etiologies. Most importantly, this work represents an international collaboration (Korea‐UK) to develop a digital twin neural marker using large datasets while upholding data democracy principles.

Background Dementia has been classified as major neurocognitive disorder and it typically presented with substantial impairment in at least one cognitive domain, interfering with day‐to‐day activities and if the impairment was moderate and yet to interfere severely with activities, it would be diagnosed as mild neurocognitive disorder. This study aims to evaluate the sensitivity and specificity of MoCA to determine its suitability as a screening tool in screening programs. Methods The study analyzed data from participants aged 55 and older, recruited from U.S. Alzheimer's Disease Research Centers (ADRCs), using a National Alzheimer Coordinating Center Uniformed Data Set (NACC‐UDS). Participants were classified based on patient records into demented and non‐demented groups, with the non‐demented group further categorized into those with normal cognition and cognitive impairment (CI). Results The study utilized an initial dataset of 188,700 participant records from NACC. After applying inclusion criteria, 16,309 participants were included. The participants had complete diagnostic information, clinician‐conducted cognitive assessments, and MoCA scores. The participants were categorized into three groups: 7,624 with no cognitive impairment (NoCI), 4,893 with MCI, and 3,792 with dementia. The optimum cutoff scores against NoCI as calculated by the Youden index were less than 24 for detecting MCI, sensitivity 77 % (95% CI, 76‐78), specificity 69 % (95%CI, 67‐69), cutoff scores against MCI as calculated by the Youden index were less than 19 for detecting dementia, sensitivity 72% (95% CI, 70‐73), specificity 80 % (95% CI, 79‐81), and cutoff scores against NoCI as calculated by the Youden index were less than 21 for detecting dementia, sensitivity 83% (95% CI, 82‐85), specificity 82 % (95% CI, 81‐83). Although PPV was generally low, the high NPV across comparisons underscores the MoCA's effectiveness in ruling out cognitive impairment. Conclusion The study confirms MoCA as an effective tool for detecting dementia, showing 83% sensitivity and 82% specificity at a cutoff value of 21. With a high NPV of 94%, MoCA is particularly reliable for ruling out dementia. Its ability to identify MCI is moderate, with a sensitivity of 77.3% at cutoff of 24.

Childhood maltreatment represents a complex stressor, with the developmental timing, duration, frequency, and type of maltreatment varying with each child (Barnett, Manly, & Cicchetti, 1993; Cicchetti & Manly, 2001). Multiple brain regions and neural circuits are disrupted by the experience of child maltreatment (Cicchetti & Toth, in press; DeBellis et al., 2002; McCrory & Viding, 2010; Teicher, Anderson, & Polcari, 2012). These neurobiological compromises indicate the impairment of a number of important cognitive functions, including working memory and inhibitory control. The present study extends prior research by examining the effect of childhood maltreatment on neurocognitive functioning based on developmental timing of maltreatment, including onset, chronicity, and recency, in a sample of 3- to 9-year-old nonmaltreated (n = 136) and maltreated children (n = 223). Maltreated children performed more poorly on inhibitory control and working-memory tasks than did nonmaltreated children. Group differences between maltreated children based on the timing of maltreatment and the chronicity of maltreatment also were evident. Specifically, children who were maltreated during infancy, and children with a chronic history of maltreatment, exhibited significantly poorer inhibitory control and working-memory performance than did children without a history of maltreatment. The results suggest that maltreatment occurring during infancy, a period of major brain organization, disrupts normative structure and function, and these deficits are further instantiated by the prolonged stress of chronic maltreatment during the early years of life.

Numerous studies have argued that bilingualism has effects on cognitive functions. Recently, in light of increasingly mixed empirical results, this claim has been challenged. One might ponder if there is enough evidence to justify a cessation to future research on the topic or, alternatively, how the field could proceed to better understand the phantom-like appearance of bilingual effects. Herein, we attempt to frame this appearance at the crossroads of several factors such as the heterogeneity of the term ‘bilingual’, sample size effects, task effects, and the complex dynamics between an early publication bias that favours positive results and the subsequent Proteus phenomenon. We conclude that any definitive claim on the topic is premature and that research must continue, albeit in a modified way. To this effect, we offer a path forward for future multi-lab work that should provide clearer answers to whether bilingualism has neurocognitive effects, and if so, under what conditions.

Schizophrenia is characterized by significant heterogeneity in outcome. The last decades have witnessed a significant interest in identifying factors that can moderate or influence clinical and functional outcomes in people with schizophrenia. One factor of particular interest is neurocognition, as performance on various measures of cognitive abilities, such as memory, attention, and executive functions, have been consistently related to functional outcome and, to a lesser extent, clinical outcome. This review aims to provide an up-to-date description of recent studies examining the association between neurocognition and clinical and (or) functional outcomes. In the first section, studies examining neurocognitive performance in relation to clinical outcome are examined. When clinical outcome is defined dichotomously (for example, comparing remitted and nonremitted), verbal memory performance consistently exhibits a strong association with clinical status, with the poor outcome group showing the largest deficits. In the second section, studies exploring the relation between neurocognition and various dimensions of functional outcome are reviewed. These dimensions include independent living, social functioning, and vocational functioning, among others. Again, a strong link between neurocognitive deficits and impairments in several aspects of functioning clearly emerges from this review. Finally, several measurement issues are discussed that pertain to the need to standardize definitions of clinical and (or) functional outcomes, the importance of defining cognitive domains consistently across studies, and distinguishing between one's competence to perform tasks and what one actually does in everyday life. Addressing these measurement issues will be key to studies examining the development of effective interventions targeting neurocognitive functions and their impact on clinical and functional outcomes.