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Background: We present a case report on the efficacy of the short-term application of vortioxetine in managing winter depression in patients with seasonal bipolar disorder (BP). Standard treatment strategies for BP may not adequately address seasonal depressive symptoms during winter in patients with seasonal BP patterns. Depressive symptoms during winter may be linked to seasonal changes in serotonin transporter binding, such as a decrease in synaptic serotonin levels, necessitating alternative approaches. Although antidepressants, including vortioxetine, are effective in treating seasonal monopolar depression, their efficacy and safety in treating depression in patients with seasonal BP patterns remain unclear. Case Presentation: This case report focuses on a 44-year-old male patient diagnosed with seasonal BP who had recurrent depressive episodes, specifically during winter. Notably, the patient had a significant decrease in recurrent episodes after short-term seasonal vortioxetine use without inducing mania or rapid cycling. Conclusion: Our study highlights the potential effectiveness of a seasonal, short-term treatment strategy with antidepressants, including vortioxetine, for winter depression in individuals with BP.
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Aim: While moderate smartphone use contributes to information gathering and relationship building, excessive smartphone use, also referred to as problematic smartphone use (PSU), has raised concerns because of its addictive nature and associated health consequences. This study aimed to investigate the relationship between treatment readiness and prognosis in individuals with PSU and to assess the predictive ability of smartphone log data in evaluating treatment readiness. Methods: A sample of 47 patients with PSU participated in this study. Treatment readiness was assessed using the Stages of Change, Readiness, and Treatment Eagerness Scale (SOCRATES), and log data were collected using a smartphone log application. Results: The results showed a significant correlation between baseline SOCRATES scores and the difference in Global Assessment of Functioning scores between baseline and 6 months (Spearman's ρ = 0.640, P-value = .001), suggesting that treatment readiness may explain part of the treatment outcomes (Pearson's r 2 = 0.379, P-value = 0.032). In addition, baseline log data, including the log acquisition rate, showed a positive correlation with treatment readiness (Spearman's ρ = 0.328, P-value = 0.045). Conclusion: These findings provide valuable insights into the relationship between treatment readiness and clinical outcomes in patients with PSU, and suggest the potential of log data as objective indicators of treatment motivation.
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Introduction: Acquired hepatocerebral degeneration (AHD) is a neurological condition associated with cerebral manganese (Mn) accumulation caused by portosystemic shunts (PSS), usually because of advanced liver disease. AHD is diagnosed by the identification of T1-weighted brain magnetic resonance imaging (MRI) hyperintensities coupled with the presence of PSS and neurological symptoms. Clinical presentations primarily involve motor dysfunction and cognitive impairment. As a result of the frequently concurrent hepatic encephalopathy, the psychiatric symptoms of AHD alone remain unclear. This report is the first documentation of unique psychiatric symptoms of AHD due to a congenital PSS (CPSS) and suggests the efficacy of shunt embolization in achieving sustained remission of psychiatric symptoms in such cases. Methods: A 57-year-old Japanese woman presented with recurrent severe depression, pain, and somatosensory hallucinations, along with fluctuating motor dysfunction, including parkinsonism, and cognitive impairments. Psychiatric interventions, including antidepressants, antipsychotics or electroconvulsive therapy, had limited efficacy or did not prevent relapse. Results: T1-weighted MRI showed bilateral hyperintensity in the globus pallidus. No history of Mn exposure or metabolic abnormalities, including copper, was identified. Furthermore, no evidence of liver dysfunction or hyperammonemia was found. Eventually, a gastrorenal shunt was observed on contrast-enhanced abdominal computed tomography. The diagnosis of AHD due to CPSS was made based on the clinical manifestations and abnormal imaging findings. Shunt embolization was performed, which prevented the relapse of psychiatric symptoms and substantially reduced the T1-weighted MRI hyperintensities. Conclusions: This case highlights the potential involvement of AHD in adult-onset psychiatric symptoms, even in the absence of liver disease. Furthermore, this case underscores the efficacy of shunt embolization in treating the psychiatric symptoms of AHD due to CPSS.
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Excessive gaming can impair both mental and physical health, drawing widespread public and clinical attention, especially among young generations. People are now more exposed to gaming-related content on social media than before, and this exposure may have a significant impact on their behavior. However, the neural mechanisms underlying this effect remain unexplored. Using functional magnetic resonance imaging (fMRI), this study aimed to investigate the neural activity induced by gaming-related content on social media among young adults casually playing online games. While being assessed by fMRI, the participants watched gaming-related videos and neutral (nongaming) videos on social media. The gaming-related cues significantly activated several brain areas, including the medial prefrontal cortex, posterior cingulate cortex, hippocampus, thalamus, superior/middle temporal gyrus, precuneus and occipital regions, compared with the neutral cues. Additionally, the participants' gaming desire levels positively correlated with a gaming-related cue-induced activation in the left orbitofrontal cortex and the right superior temporal gyrus. These findings extend previous studies on gaming cues and provide useful information to elucidate the effects of gaming-related content on social media in young adults. Continued research using real-world gaming cues may help improve our understanding of promoting gaming habits and provide support to individuals vulnerable to gaming addiction.
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Mapeo Encefálico , Encéfalo , Señales (Psicología) , Imagen por Resonancia Magnética , Medios de Comunicación Sociales , Juegos de Video , Humanos , Adulto Joven , Masculino , Encéfalo/fisiología , Encéfalo/diagnóstico por imagen , Femenino , Adulto , Conducta Adictiva/fisiopatología , AdolescenteRESUMEN
Introduction: Excessive daytime sleepiness (EDS) is a crucial symptom that diminishes the quality of life. The primary causes of EDS are central hypersomnia, including narcolepsy type 1 (NT1), type 2 (NT2), and idiopathic hypersomnia (IH). EDS is often associated with other psychiatric disorders, particularly attention deficit hyperactivity disorder (ADHD). The Multiple Sleep Latency Test (MSLT) is the standard assessment tool for EDS. Although the MSLT yields numerous parameters, most are not employed in clinical practice. In this study, we leveraged novel MSLT parameters to discern central hypersomnia and ADHD presence. Our analysis focused on sleep latency variability and employed cluster analysis to identify unique temporal patterns. Methods: We examined the MSLT data from 333 patients; of these, 200 (aged 14-54, mean: 24.9 ± 8.1, years; 114 females) met the inclusion criteria comprising comprehensive data an Apnea-Hypopnea Index (AHI) below 5, and no prior diagnosis of sleep apnea syndrome. We employed a time-course cluster approach that specifically targeted sleep latency variability during the MSLT. Results: Considering both multiple clustering quality evaluations and the study's objectives, we identified 9 distinct clusters. Clusters 1 and 3 predominantly had MSLT-positive results; Cluster 2 was entirely MSLT-positive; Clusters 4, 5, 6, 8, and 9 were mainly MSLT-negative; and Cluster 7 had mixed results. The diagnosis of hypersomnia varied notably among Clusters 1, 2, 3, and 7, with Cluster 2 demonstrating a pronounced tendency towards NT1 and NT2 diagnoses (p < 0.005). However, no significant correlation was observed between ADHD diagnoses and specific sleep latency patterns in any cluster. Conclusions: Our study highlights the value of time-course clustering in understanding sleep latency patterns of patients with central hypersomnia.
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Several studies have shown white matter (WM) dysconnectivity in people with schizophrenia (SZ). However, the underlying mechanism remains unclear. We investigated the relationship between plasma homocysteine (Hcy) levels and WM microstructure in people with SZ using diffusion tensor imaging (DTI). Fifty-three people with SZ and 83 healthy controls (HC) were included in this retrospective observational study. Tract-Based Spatial Statistics (TBSS) were used to evaluate group differences in WM microstructure. A significant negative correlation between plasma Hcy levels and WM microstructural disruption was noted in the SZ group (Spearman's ρ = -.330, P = 0.016) but not in the HC group (Spearman's ρ = .041, P = 0.712). These results suggest that increased Hcy may be associated with WM dysconnectivity in SZ, and the interaction between Hcy and WM dysconnectivity could be a potential mechanism of the pathophysiology of SZ. Further, longitudinal studies are required to investigate whether high Hcy levels subsequently cause WM microstructural disruption in people with SZ.
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AIM: While conservatism bias refers to the human need for more evidence for decision-making than rational thinking expects, the jumping to conclusions (JTC) bias refers to the need for less evidence among individuals with schizophrenia/delusion compared to healthy people. Although the hippocampus-midbrain-striatal aberrant salience system and the salience, default mode (DMN), and frontoparietal networks ("triple networks") are implicated in delusion/schizophrenia pathophysiology, the associations between conservatism/JTC and these systems/networks are unclear. METHODS: Thirty-seven patients with schizophrenia and 33 healthy controls performed the beads task, with large and small numbers of bead draws to decision (DTD) indicating conservatism and JTC, respectively. We performed independent component analysis (ICA) of resting functional magnetic resonance imaging (fMRI) data. For systems/networks above, we investigated interactions between diagnosis and DTD, and main effects of DTD. We similarly applied ICA to structural and diffusion MRI to explore the associations between DTD and gray/white matter. RESULTS: We identified a significant main effect of DTD with functional connectivity between the striatum and DMN, which was negatively correlated with delusion severity in patients, indicating that the greater the anti-correlation between these networks, the stronger the JTC and delusion. We further observed the main effects of DTD on a gray matter network resembling the DMN, and a white matter network connecting the functional and gray matter networks (all P < 0.05, family-wise error [FWE] correction). Function and gray/white matter showed no significant interactions. CONCLUSION: Our results support the novel association of conservatism and JTC biases with aberrant salience and default brain mode.
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Toma de Decisiones , Red en Modo Predeterminado , Deluciones , Imagen por Resonancia Magnética , Esquizofrenia , Humanos , Adulto , Red en Modo Predeterminado/fisiopatología , Red en Modo Predeterminado/diagnóstico por imagen , Masculino , Femenino , Esquizofrenia/fisiopatología , Esquizofrenia/diagnóstico por imagen , Deluciones/fisiopatología , Deluciones/diagnóstico por imagen , Toma de Decisiones/fisiología , Red Nerviosa/diagnóstico por imagen , Red Nerviosa/fisiopatología , Sustancia Blanca/diagnóstico por imagen , Sustancia Blanca/fisiopatología , Sustancia Blanca/patología , Persona de Mediana Edad , Adulto Joven , Cuerpo Estriado/diagnóstico por imagen , Cuerpo Estriado/fisiopatología , Sustancia Gris/diagnóstico por imagen , Sustancia Gris/fisiopatología , Sustancia Gris/patologíaRESUMEN
Excessive gameplay can have negative effects on both mental and physical health, especially among young people. Nowadays, social media platforms are bombarding users with gaming-related content daily. Understanding the effect of this content on people's behavior is essential to gain insight into problematic gaming habits. However, this issue is yet to be studied extensively. In this study, we examined how gaming-related content on social media affects young adults explicitly and implicitly. We studied 25 healthy young adults (average age 21.5 ± 2.2) who played online games casually and asked them to report their gaming desire. We also conducted an implicit association test (IAT) to measure their implicit attitudes toward gaming-related content. We also investigated the relationship between these measures and various psychological factors, such as personality traits, self-efficacy, impulsiveness, and cognitive flexibility. The results revealed that participants had a higher explicit gaming desire when exposed to gaming-related cues on social media than neutral cues. They also had a robust positive implicit attitude toward gaming-related content on social media. Explicit gaming desire was positively correlated with neuroticism levels. Furthermore, the IAT effect was negatively correlated with self-efficacy and cognitive flexibility levels. However, there were no significant correlations between explicit gaming desire/IAT effect and impulsiveness levels. These findings suggest that gaming-related content on social media can affect young adults' behavior both explicitly and implicitly, highlighting the need for further research to prevent gaming addiction in vulnerable individuals.
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Inosine monophosphate dehydrogenase (IMPDH) is a rate-limiting enzyme in the de novo GTP biosynthesis pathway. Recent studies suggest that IMPDH2, an isoform of IMPDH, can localize to specific subcellular compartments under certain conditions and regulate site-specific GTP availability and small GTPase activity in invasive cancer cells. However, it is unclear whether IMPDH2 plays a site-specific regulatory role in subcellular functions in healthy cells. In this study, we focused on brain cells and examined the localization pattern of IMPDH2. We discovered that IMPDH2 forms localized spots in the astrocytes of the adult mouse hippocampus. Further analysis of spot distribution in primary astrocyte cultures revealed that IMPDH2 spots are predominantly localized on branching sites and distal ends of astrocyte stem processes. Our findings suggest a potential unidentified role for IMPDH2 and GTP synthesis specifically at specialized nodes of astrocyte branches.
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Astrocitos , IMP Deshidrogenasa , Animales , Ratones , Astrocitos/metabolismo , Guanosina Trifosfato , IMP Deshidrogenasa/genética , IMP Deshidrogenasa/metabolismo , IMP Deshidrogenasa/ultraestructura , Isoformas de ProteínasRESUMEN
Childhood abuse reduces hippocampal and amygdala volumes and impairs social cognition, including the ability to recognize facial expressions. However, these associations have been studied primarily in individuals with a history of severe abuse and psychiatric symptoms; researchers have not determined whether these associations can also be observed in healthy adults. In the present study, we analyzed data from 400 healthy adults (208 men and 192 women) at Tamagawa University. Parental rejection reflecting childhood abuse was assessed using the short form of Egna Minnen Beträffande Uppfostran, while social cognition was assessed using the "Fake Smile Detection Task." Hippocampal and amygdala volumes were extracted from T1-weighted magnetic resonance imaging data using FreeSurfer. We found that greater parental rejection resulted in smaller hippocampal and amygdala volumes and poorer performance in the Fake Smile Detection Task. Structural equation modeling analysis supported the model that hippocampal volume mediates maternal rejection effect on performance on the Fake Smile Detection Task, with involvement of the amygdala. These findings are in line with the structural and functional connectivity found between the hippocampus and amygdala and their joint involvement in social cognition. Therefore, parental rejection may affect hippocampal and amygdala volumes and social cognitive function even in symptom-free adults.
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Imagen por Resonancia Magnética , Cognición Social , Masculino , Humanos , Adulto , Femenino , Niño , Imagen por Resonancia Magnética/métodos , Hipocampo/patología , Amígdala del Cerebelo , CogniciónRESUMEN
Background: Evidence regarding the effectiveness of melatonin receptor agonists in treating delayed sleep-wake phase disorder (DSWPD) remains limited. This study aimed to determine the optimal dose of ramelteon, a melatonin receptor agonist, for the better treatment adherence of DSWPD. Methods: The patients who were diagnosed definitely as having DSWPD by board-certified physicians specialized in sleep medicine and started to receive strategically timed ramelteon medications after the diagnosis were included. Data on the initial ramelteon dose and follow-up duration (up to 24 months) were collected retrospectively. Patients with treatment discontinuation, changes in ramelteon dose, or the addition of other sleep-related medications were considered dropouts. Kaplan-Meier estimates, log-rank tests, and Cox regression analyses were performed. Results: Overall, 373 patients were analyzed. The findings revealed that the 2 mg dose of ramelteon was associated with a lower dropout rate compared to the other doses (8 mg, 4 mg, and 1 mg). The dropout rate for the 2 mg group was estimated to have a hazard ratio (HR) of 0.5762 when compared with the 8 mg dose group. Sex did not reveal a significant HR, whereas older age exhibited a small but significant HR (0.9858). Conclusion: For achieving better adherence, a dosing regimen of strategically timed 2 mg ramelteon may be the best for the treatment of DSWPD. The therapeutic dose window for better adherence seems to center approximately 2 mg of ramelteon. Furthermore, caution should be exercised when treating younger patients to prevent dropouts.
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Chronic kidney disease (CKD) causes cognitive impairment and contributes to the overall global burden of dementia. However, mechanisms through which the kidneys and brain communicate are not fully understood. We established a CKD mouse model through adenine-induced tubulointerstitial fibrosis. Novel object recognition tests indicated that CKD decreased recognition memory. Sarkosyl-insoluble-proteomic analyses of the CKD mouse hippocampus revealed an accumulation of insoluble MAPT (microtubule-associated protein tau) and RNA-binding proteins such as small nuclear ribonucleoprotein U1 subunit 70 (SNRNP70). Additionally, there was an accumulation of Immunoglobulin G (IgG), indicating blood-brain barrier (BBB) breakdown. We identified that expressions of essential tight-junction protein claudin-5 and adherens-junction protein platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) were decreased in the brain endothelial cells of CKD mice. We determined urea as a major uremic solute that dose dependently decreased both claudin-5 and PECAM-1 expression in the mouse brain endothelial cell line bEnd.3 cells. Gelatin zymography indicated that the serum of CKD mice activated matrix metalloproteinase-2 (MMP2), while marimastat ameliorated the reduction of claudin-5 expression by urea in bEnd.3 cells. This study established a brain proteomic signature of CKD indicating BBB breakdown and insolubility of tau protein, which are pathologically linked to Alzheimer's disease. Urea-mediated activation of MMP2 was partly responsible for BBB breakdown in CKD.
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Barrera Hematoencefálica , Insuficiencia Renal Crónica , Animales , Ratones , Barrera Hematoencefálica/metabolismo , Claudina-5/metabolismo , Células Endoteliales/metabolismo , Metaloproteinasa 2 de la Matriz/metabolismo , Molécula-1 de Adhesión Celular Endotelial de Plaqueta , Proteómica , Insuficiencia Renal Crónica/metabolismo , Proteínas tau/metabolismoRESUMEN
BACKGROUND: Epilepsy causes substantial psychological distress and anxiety, primarily due to seizures. However, the impact of stress responses and changes in arousal and their association with anxiety patterns in patients with epilepsy (PWE) remains unclear. This study aimed to investigate the relationships among seizures, stress and arousal characteristics, and trait and state anxiety characteristics in PWE. METHODS: Our sample consisted of 159 outpatients with epilepsy recruited from five institutions in Japan in 2020. Participants completed the State-Trait Anxiety Inventory-Form JYZ (STAI) and the Japanese-Stress Arousal Check List (J-SACL). We analyzed the correlations between inventory scores and clinical information. Using principal component analysis (PCA), we derived epilepsy-specific stress/arousal characteristics, which accounted for high arousal and low-stress levels, termed epilepsy-specific stress or arousal response (ESAR), from the J-SACL scores. We conducted a mediation analysis to assess the mediating role of ESAR in the relationship between traits and state anxiety. RESULTS: We found significant correlations between J-SACL stress and arousal factors (r = -0.845, p < 0.001), ESAR and seizure frequency (r = -0.29, p < 0.001), ESAR and trait anxiety scores on the STAI (r = -0.77, p < 0.0001), and ESAR and state anxiety scores on the STAI (r = -0.60, p < 0.0001). Mediation analysis supported by the Monte Carlo method revealed that ESAR significantly mediated the association between trait and state anxiety. CONCLUSIONS: These findings elucidate the epilepsy-specific stress and arousal characteristics and their roles in mediating traits and state anxiety. These results may reflect the long-term clinical course and unique emotion recognition tendencies in epilepsy.
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Individuals with autism spectrum disorder (ASD) often show limited empathy (poor recognition of others' emotions) and high alexithymia (poor recognition of own emotions and external thinking), which can negatively impact their social functioning. Previous experimental studies suggest that alterations in cognitive flexibility play key roles in the development of these characteristics in ASD. However, the underlying neural mechanisms that link cognitive flexibility and empathy/alexithymia are still largely unknown. In this study, we examined the neural correlates of cognitive flexibility via functional magnetic resonance imaging during perceptual task-switching in typical development (TD) adults and adults with ASD. We also investigated associations between regional neural activity and psychometric empathy and alexithymia scores among these populations. In the TD group, stronger activation of the left middle frontal gyrus was associated with better perceptual switching and greater empathic concern. Among individuals with ASD, stronger activation of the left inferior frontal gyrus was associated with better perceptual switching, greater empathy, and lower alexithymia. These findings will contribute to develop a better understanding of social cognition, and could be informative for the development of new ASD therapies.
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Trastorno del Espectro Autista , Empatía , Adulto , Humanos , Síntomas Afectivos/diagnóstico por imagen , Síntomas Afectivos/etiología , Trastorno del Espectro Autista/diagnóstico por imagen , Trastorno del Espectro Autista/psicología , Emociones/fisiología , Lóbulo Frontal , Imagen por Resonancia MagnéticaRESUMEN
Increased excitatory neuronal tones have been implicated in autism, but its mechanism remains elusive. The amplified glutamate signals may arise from enhanced glutamatergic circuits, which can be affected by astrocyte activation and suppressive signaling of dopamine neurotransmission. We tested this hypothesis using magnetic resonance spectroscopy and positron emission tomography scan with 11C-SCH23390 for dopamine D1 receptors in the anterior cingulate cortex (ACC). We enrolled 18 male adults with high-functioning autism and 20 typically developed (TD) male subjects. The autism group showed elevated glutamate, glutamine, and myo-inositol (mI) levels compared with the TD group (p = 0.045, p = 0.044, p = 0.030, respectively) and a positive correlation between glutamine and mI levels in the ACC (r = 0.54, p = 0.020). In autism and TD groups, ACC D1 receptor radioligand binding was negatively correlated with ACC glutamine levels (r = - 0.55, p = 0.022; r = - 0.58, p = 0.008, respectively). The enhanced glutamate-glutamine metabolism might be due to astroglial activation and the consequent reinforcement of glutamine synthesis in autistic brains. Glutamine synthesis could underly the physiological inhibitory control of dopaminergic D1 receptor signals. Our findings suggest a high neuron excitation-inhibition ratio with astrocytic activation in the etiology of autism.
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Trastorno Autístico , Glutamina , Masculino , Adulto , Humanos , Glutamina/metabolismo , Ácido Glutámico/metabolismo , Trastorno Autístico/metabolismo , Astrocitos/metabolismo , Dopamina/metabolismo , Encéfalo/diagnóstico por imagen , Encéfalo/metabolismo , Giro del Cíngulo/diagnóstico por imagen , Giro del Cíngulo/metabolismoRESUMEN
Although mitigating burnout has long been a pressing issue in healthcare, recent global disasters, including the COVID-19 pandemic and wars, have exacerbated this problem. Medical professionals are frequently exposed to diverse job-induced distress; furthermore, the importance of people's sense of coherence (SOC) over work has been addressed to better deal with burnout. However, the neural mechanisms underlying SOC in medical professionals are not sufficiently investigated. In this study, the intrinsic fractional amplitude of low-frequency fluctuations (fALFF) were measured as an indicator of regional brain spontaneous activity using resting-state functional magnetic resonance imaging in registered nurses. The associations between participants' SOC levels and the fALFF values within brain regions were subsequently explored. The SOC scale scores were positively correlated with fALFF values in the right superior frontal gyrus (SFG) and the left inferior parietal lobule. Furthermore, the SOC levels of the participants mediated the link between their fALFF values in the right SFG and the depersonalization dimension of burnout. The results deepened the understanding of the counter role of SOC on burnout in medical professionals and may provide practical insights for developing efficient interventions.
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COVID-19 , Sentido de Coherencia , Humanos , Pandemias , Corteza Prefrontal , Agotamiento PsicológicoRESUMEN
Autism spectrum disorder (ASD) is a lifelong condition, and its underlying biological mechanisms remain elusive. The complexity of various factors, including inter-site and development-related differences, makes it challenging to develop generalizable neuroimaging-based biomarkers for ASD. This study used a large-scale, multi-site dataset of 730 Japanese adults to develop a generalizable neuromarker for ASD across independent sites and different developmental stages. Our adult ASD neuromarker achieved successful generalization for the US and Belgium adults and Japanese adults. The neuromarker demonstrated significant generalization for children and adolescents. We identified 141 functional connections (FCs) important for discriminating individuals with ASD from TDCs. Finally, we mapped schizophrenia (SCZ) and major depressive disorder (MDD) onto the biological axis defined by the neuromarker and explored the biological continuity of ASD with SCZ and MDD. We observed that SCZ, but not MDD, was located proximate to ASD on the biological dimension defined by the ASD neuromarker. The successful generalization in multifarious datasets and the observed relations of ASD with SCZ on the biological dimensions provide new insights for a deeper understanding of ASD.
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Although numerous studies have focused on brain functions related to inequity aversion, few have examined its genetic basis. Here, we show the association between estimated inequity aversion and polymorphisms in three genes associated with human sociality. Non-student adult participants took part in five economic game experiments on different days. Disadvantageous inequity aversion (DIA) and advantageous inequity aversion (AIA) were calculated from behavioural responses using Bayesian estimation. We investigated the association between genetic polymorphisms in the oxytocin receptor (OXTR rs53576), arginine vasopressin receptor 1A (AVPR1A RS3) and opioid receptor mu 1 (OPRM1 rs1799971) and inequity aversion. Regarding AVPR1A RS3, participants with the SS genotype had higher AIA than those with the SL or LL genotypes, but no association was found for DIA. Moreover, we observed no aversion associations for OXTR rs53576 or OPRM1 rs1799971. The results suggest that AVPR1A plays an important role in aversion when one's own gain is greater than that of others. Our findings may provide a solid theoretical basis for future studies on the relationship between genetic polymorphisms and inequity aversion.
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Afecto , Receptores de Vasopresinas , Adulto , Humanos , Teorema de Bayes , Receptores de Vasopresinas/genética , Genotipo , Polimorfismo GenéticoRESUMEN
In the context of discovery of synaptic autoantibodies in patients with encephalitis, autoimmune psychosis with acute encephalopathy and psychosis as the main symptom has been proposed on the basis of those autoantibodies. Correspondingly, autoantibody-related mechanisms have also been proposed in schizophrenia. This paper outlines the relationship between schizophrenia and autoimmune psychosis by describing the relationship between synaptic autoantibodies and schizophrenia and our findings regarding anti-NCAM1 autoantibodies in schizophrenia.