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IntroductionPathophysiological etiology of schizophrenia remains unclear due to the heterogeneous nature of its biological and clinical manifestations. Dysfunctional communication among large-scale brain networks and hub nodes have been reported. In this study, an exploratory approach was adopted to evaluate the dysfunctional connectome of brain in schizophrenia.MethodsTwo hundred adult individuals with schizophrenia and 200 healthy controls were recruited from Taipei Veterans General Hospital. All subjects received functional magnetic resonance imaging (fMRI) scanning. Functional connectivity (FC) between parcellated brain regions were obtained. Pair-wise brain regions with significantly different functional connectivity among the two groups were identified and further analyzed for their concurrent ratio of connectomic differences with another solitary brain region (single-FC dysfunction) or dynamically interconnected brain network (network-FC dysfunction).ResultsThe right thalamus had the highest number of significantly different pair-wise functional connectivity between schizophrenia and control groups, followed by the left thalamus and the right middle frontal gyrus. For individual brain regions, dysfunctional single-FCs and network-FCs could be found concurrently. Dysfunctional single-FCs distributed extensively in the whole brain of schizophrenia patients, but overlapped in similar groups of brain nodes. A dysfunctional module could be formed, with thalamus being the key dysfunctional hub.DiscussionThe thalamus can be a critical hub in the brain that its dysfunctional connectome with other brain regions is significant in schizophrenia patients. Interconnections between dysfunctional FCs for individual brain regions may provide future guide to identify critical brain pathology associated with schizophrenia.

Aim: Bipolar disorder (BD) and major depression have been associated with an increased risk of developing Parkinson's disease (PD); however, few studies have directly compared the risk of PD development between patients with BD and major depression while considering relevant risk factors and psychotropic medications. Methods: Using the Taiwan National Health Insurance Research Database, 21,186 patients with BD, 21,188 patients with major depression, and 42,374 controls were enrolled between 2001 and 2009, and followed until the end of 2011. Individuals who developed PD during the follow‐up period were identified. Cox regression models were used to analyze the hazard ratio (HR) of developing PD, adjusting for demographic factors, comorbidities, and psychotropic medication usage. Results: Both patients with BD [HR 8.63, 95% confidence interval (CI) 6.35–11.72] and those with major depression (HR 5.68, 95% CI 4.15–7.78) had an elevated risk of subsequent PD compared to the controls. Patients with BD were associated with a 51% increased risk of subsequent PD compared with patients with major depression. Long‐term treatment with antiepileptic mood stabilizers was associated with increased PD risk among patients with late‐onset BD and high Charlson comorbidity index scores. Lithium was not associated with an increased PD risk. Conclusions: The study highlights an elevated PD risk in patients with BD and major depression compared to the controls, with BD patients at highest risk. Further research is needed to elucidate the complex interplay between psychotropic medications and neurodegenerative processes in BD, aiming to optimize therapeutic strategies and improve patient outcomes. [ABSTRACT FROM AUTHOR]

Background: Sleep disturbance and impulsivity are key components of mood vulnerability in bipolar disorder (BD), but few studies have assessed the association between these two symptoms among patients with BD. Methods: Forty-seven euthymic patients with bipolar I disorder (BDI) or bipolar II disorder (BDII) and 58 age- and sex-matched healthy controls were enrolled in this cross-sectional study. Trait impulsivity was measured using the Barratt Impulsiveness Scale Version 11 (BIS-11), which yielded 3 second-order factors: attention, motor, and non-planning. Subjective sleep quality was assessed using the self-reported Pittsburgh Sleep Quality Index (PSQI). General linear models (GLMs) were used to assess the associations between subjective poor sleep and trait impulsivity with multiple testing corrections. Results: Patients with BD scored higher in BIS-11 and PSQI than healthy controls. PSQI total scores positively correlated with BIS-11 total scores, while sleep disturbance and daytime dysfunction were associated with attentional impulsiveness after controlling for covariates. Participants with higher PSQI total scores (>10) had higher scores in BIS-11 total, attention, and non-planning than those with low PSQI scores (≤5). Conclusion: These findings support the hypothesis that poor sleep quality might lead to impulsivity and add to the growing evidence that improving sleep quality may be a therapeutic target for patients with BD. [ABSTRACT FROM AUTHOR]

Copyright of Tijdschrift voor Jeugdrecht is the property of Boom uitgevers Den Haag and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Tijdschrift voor Jeugdrecht is the property of Boom uitgevers Den Haag and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Because of a relative dearth of longitudinal studies, the directionality of the relationship between mood and inflammation among patients with bipolar disorder (BD) is still unclear. We aimed to investigate the longitudinal associations of pro‐inflammatory markers with mood symptom severity in BD. Methods: Hundred and thirty‐two adult patients with BD were enrolled. At the baseline and 1‐year follow‐up visit, all participants received mood assessment with Montgomery Åsberg depression rating scale (MADRS) and Young mania rating scale, and underwent blood draws to quantify metabolic profile and serum levels of the pro‐inflammatory markers, including soluble interleukin‐6 receptor, soluble tumor necrosis factor‐α receptor type 1 (sTNF‐αR1), monocyte chemoattractant protein‐1, and C‐reactive protein. A four‐factor model of MADRS, consisting of sadness, negative thoughts, detachment, and neurovegetative symptoms, were applied. Results: At baseline, 65 patients with BD were in depressed state, and 67 patients with BD were in euthymic state. Among patients in depressed state, baseline MADRS total score positively correlated with sTNF‐αR1 level at follow‐up. While baseline sTNF‐αR1 level positively predicted sadness symptom in euthymic patients with BD who later developed depression (n = 22), sadness in patients with bipolar depression predicted later increase in serum sTNF‐αR1 level even after remission (n = 17). Moreover, lithium had a stronger effect of lowering peripheral sTNF‐αR1 level as compared with other mood stabilizers. Conclusion: Our results indicate the bidirectional inflammation‐depression relationship in BD. [ABSTRACT FROM AUTHOR]

Objectives: To investigate potential risk factors for mild behavioral impairment (MBI) among non-demented geriatrics. Design: Population-based, cross-sectional survey. Setting: Taiwan Alzheimer Disease Association (TADA) Database. Participants: Participants were selected by multistage random sampling of all Taiwan counties. They received in-person interviews between December 2011 and March 2013. Measurements: Demographic data, lifestyle and habits, medical comorbidities, cognitive status measured by the Taiwanese Mini-Mental Status Examination (TMSE) and presence of MCI of the participants were collected. Subjects were distributed to the MBI and non-MBI groups. These factors had been evaluated for their effects on MBI in the univariate and multivariable logistic regression models. Results: In total, 6,196 non-demented participants aged 65 years or older, including 409 MBI and 5,787 non-MBI participants, were recruited. After adjustment for age, sex, education, body mass index, lifestyle and habits, medical comorbidities, and MCI, good sleep was associated with lower risk of MBI (OR 0.09, 95% CI 0.07 – 0.12). Low body weight (OR 2.01, 95% CI 1.21–3.33), low-to-medium education (OR 1.40, 95%CI 1.06–1.85; OR 2.32, 95% CI 1.67–3.21), medical comorbidities of hypertension (OR 1.56, 95% CI 1.25–1.95), hyperlipidemia (OR 1.29, 95% CI 1.00–1.67), cancer (OR 2.05, 95% CI 1.37–3.06) were significantly associated with increased MBI risk. MCI neither increased nor decreased risk of MBI (OR 1.00, 95% CI 0.76–1.32). Conclusions: Good sleep was associated with lower MBI risk. Underweight, lower education, medical comorbidities of cancer, hypertension, hyperlipidemia were predictive of MBI. [ABSTRACT FROM AUTHOR]

Reference 1 Chan, Y.-L., Cheng, C.-M., Huang, M.-H., Lee, H.-J., Tang, L.-Y., and Tsai, C.-F. (2021). Risk factors for mild behavioral impairment in non-demented geriatrics: a population-based survey in Taiwan - RETRACTION I International Psychogeriatrics i wishes to inform its readers that it has retracted the following article: Chan, Y.-L., Cheng, C.-M., Huang, M.-H., Lee, H.-J., Tang, L.-Y., and Tsai, C.-F. (2021). [Extracted from the article]

ABSTRACT Background Methods Results Conclusion The neurobiological basis of impulsivity and its role in suicide attempt (SA) in BD remains underexplored. This study aimed to examine the functional connectivity (FC) within the prefrontal cortex (PFC) in BD patients with and without a history of SA, focusing on the role of trait impulsivity.Seventy‐two euthymic BD patients (34 with a history of SA, BDSA; and 38 without, BDNS) and 55 age‐ and sex‐matched healthy controls underwent resting‐state functional MRI. FC analyses were conducted on four PFC regions: superior frontal gyrus (SFG), middle frontal gyrus (MFG), inferior frontal gyrus (IFG), and orbitofrontal cortex (OFC). Trait impulsivity was assessed using the Barratt Impulsiveness Scale (BIS‐11), and its association with FC was analyzed using a general linear model, adjusting for demographic and clinical variables.BDSA had higher trait impulsivity than BDNS and the controls. BDSA exhibited reduced FC between the PFC and sensorimotor (postcentral and precentral gyri) and thalamic regions compared to BDNS. These reductions in FC of the fronto‐thalamic and fronto‐sensorimotor circuits were significantly associated with higher trait impulsivity scores.The findings highlight specific PFC‐based FC alterations associated with suicide attempts and trait impulsivity in BD, offering potential neurobiological markers for suicide risk in this population. [ABSTRACT FROM AUTHOR]

Background: Belzutifan, a hypoxia-inducible factor 2a inhibitor, showed clinical activity in clear-cell renal-cell carcinoma in early-phase studies. Methods: In a phase 3, multicenter, open-label, active-controlled trial, we enrolled participants with advanced clear-cell renal-cell carcinoma who had previously received immune checkpoint and antiangiogenic therapies and randomly assigned them, in a 1:1 ratio, to receive 120 mg of belzutifan or 10 mg of everolimus orally once daily until disease progression or unacceptable toxic effects occurred. The dual primary end points were progression-free survival and overall survival. The key secondary end point was the occurrence of an objective response (a confirmed complete or partial response). Results: A total of 374 participants were assigned to belzutifan, and 372 to everolimus. At the first interim analysis (median follow-up, 18.4 months), the median progression-free survival was 5.6 months in both groups; at 18 months, 24.0% of the participants in the belzutifan group and 8.3% in the everolimus group were alive and free of progression (two-sided P = 0.002, which met the prespecified significance criterion). A confirmed objective response occurred in 21.9% of the participants (95% confidence interval [CI], 17.8 to 26.5) in the belzutifan group and in 3.5% (95% CI, 1.9 to 5.9) in the everolimus group (P<0.001, which met the prespecified significance criterion). At the second interim analysis (median follow-up, 25.7 months), the median overall survival was 21.4 months in the belzutifan group and 18.1 months in the everolimus group; at 18 months, 55.2% and 50.6% of the participants, respectively, were alive (hazard ratio for death, 0.88; 95% CI, 0.73 to 1.07; two-sided P = 0.20, which did not meet the prespecified significance criterion). Grade 3 or higher adverse events of any cause occurred in 61.8% of the participants in the belzutifan group (grade 5 in 3.5%) and in 62.5% in the everolimus group (grade 5 in 5.3%). Adverse events led to discontinuation of treatment in 5.9% and 14.7% of the participants, respectively. Conclusions: Belzutifan showed a significant benefit over everolimus with respect to progression-free survival and objective response in participants with advanced clear-cell renal-cell carcinoma who had previously received immune checkpoint and antiangiogenic therapies. Belzutifan was associated with no new safety signals. (Funded by Merck Sharp and Dohme, a subsidiary of Merck; LITESPARK-005 ClinicalTrials.gov number, NCT04195750.). [ABSTRACT FROM AUTHOR]