[Psychiatric symptoms of Lewy body dementia]. / Symptômes psychiatriques de la démence à corps de Lewy.

Lewy body dementia (LBD) is the second most common neurodegenerative disorder after Alzheimer's disease. Cognitive fluctuations, visual hallucinations, parkinsonian signs, and rapid eye movement sleep behavior disorder (RBD) are diagnostic criteria. However, the diverse clinical presentations complicate diagnosis and management, as the disease may begin with psychiatric symptoms, confusion, sleep disturbances, and/or autonomic dysfunction. Its progression often leads to neuropsychiatric and behavioral symptoms that can overshadow cognitive impairments. Diagnosing LBD is crucial to avoid first iatrogenic effects (e.g., neuroleptics), and then facilitate a personalized approach to address cognitive and neuropsychiatric management, while considering comorbidities.

La démence à corps de Lewy (DCL) est la deuxième pathologie neurodégénérative la plus fréquente après la maladie d'Alzheimer. Les fluctuations cognitives, hallucinations visuelles, signes parkinsoniens, et le trouble du comportement en sommeil paradoxal (TCSP) font partie des critères diagnostics. Cependant, la diversité des présentations cliniques rend le diagnostic et la prise en charge difficiles, la maladie pouvant débuter avec des manifestations psychiatriques, confusion, troubles du sommeil et/ou dysautonomiques. Sa progression entraîne souvent des troubles neuropsychiatriques et du comportement qui peuvent prédominer sur les troubles cognitifs. Diagnostiquer la DCL permet d'abord d'éviter l'iatrogénie (par ex. neuroleptiques) et de personnaliser la prise en charge cognitive et neuropsychiatrique, en tenant compte des comorbidités.

Psychiatric disorders among survivors of childhood acute lymphoblastic leukemia in Denmark and Sweden.

BACKGROUND: The diagnosis and treatment of childhood acute lymphoblastic leukemia (ALL) may impact mental health. We investigated the long-term risk of psychiatric disorders among survivors of ALL in a population-based cohort study. METHODS: We identified patients diagnosed with ALL in Denmark and Sweden before age 20 during 1982-2008. Survivors of ALL (n = 2026), their siblings (n = 3027), and population comparison subjects (n = 9713) were followed for hospital contacts for psychiatric disorders from 5 years after ALL diagnosis (or corresponding index date) until 2017. RESULTS: By age 30, the absolute risk of psychiatric hospital contacts was 19.9% (95% confidence interval [CI]: 17.9-22.1) for ALL survivors, 18.5% (95% CI: 16.9-20.2) for siblings, and 18.3% (95% CI: 17.3-19.2) for population comparison subjects. Overall, survivors were at higher risk of any psychiatric disorders than siblings (hazard ratio [HR] = 1.25; 95% CI: 1.04-1.50), and population comparison subjects (HR = 1.20; 95% CI: 1.06-1.35). The subgroup of survivors (n = 332) who received a hematopoietic stem cell transplantation (HSCT) and/or had a relapse were at highest risk of psychiatric disorders (HR = 2.07; 95% CI: 1.26-3.41 compared to siblings; HR = 1.67; 95% CI: 1.25-2.23 compared to population comparison subjects). CONCLUSIONS: The overall absolute risk of psychiatric hospital contacts among ALL survivors was close to that in siblings and population comparison subjects. The modestly increased relative risk was mainly driven by the subgroup of survivors who received HSCT and/or had a relapse. Our findings are reassuring for the large subgroup of ALL survivors without HSCT or relapse, and provide novel insight on both absolute and relative risk of hospital contacts for psychiatric disorders.

Behavioral Assays for Comprehensive Evaluation of Cognitive and Neuropsychiatric Comorbidities of Traumatic Brain Injury and Chronic Neurological Disorders.

Neurological deficits, psychiatric disorders, and cognitive impairments often accompany stroke, brain injury, epilepsy, and many neurological disorders, which present intricate comorbidities that challenge recognition and management. There are many tools and paradigms for evaluating learning, memory, anxiety, and depression-like behaviors in lab animal models of brain disorders. However, there is a significant gap between clinical observations and experimental models, which limit understanding of the complex interplay between chronic brain conditions and their impact on cognitive dysfunction and psychiatric impairments. This article describes an overview of experimental rationale, methods, protocols, and strategies for evaluating sensorimotor, affective and cognitive-associated comorbid behaviors in epilepsy, traumatic brain injury (TBI), stroke, spinal cord injury (SCI), and many other neurological disorders. First, we delve into clinical evidence elucidating the profound impact of comorbidities, e.g., psychiatric disorders and cognitive deficits, in individuals with epilepsy. Then, we discuss diverse approaches to assess these comorbidities in experimental models of brain diseases. Finally, we explore the methodologies for assessing motor function, sensorimotor, behavior, and psychiatric health. We cover strategies and protocols enabling these assays, including implementing behavioral paradigms to assess learning and memory, anxiety, and depression-like behaviors in rodents in health and disease conditions. It is essential to consider a comprehensive battery of tests to investigate various behavioral deficits, considering environment, age, and sex differences relevant to the disease, such as TBI, SCI, epilepsy, stroke, and other complex neurological conditions. © 2024 The Author(s). Current Protocols published by Wiley Periodicals LLC.

Prenatal Stress and Ethanol Exposure: Microbiota-Induced Immune Dysregulation and Psychiatric Risks.

Changes in maternal gut microbiota due to stress and/or ethanol exposure can have lasting effects on offspring's health, particularly regarding immunity, inflammation response, and susceptibility to psychiatric disorders. The literature search for this review was conducted using PubMed and Scopus, employing keywords and phrases related to maternal stress, ethanol exposure, gut microbiota, microbiome, gut-brain axis, diet, dysbiosis, progesterone, placenta, prenatal development, immunity, inflammation, and depression to identify relevant studies in both preclinical and human research. Only a limited number of reviews were included to support the arguments. The search encompassed studies from the 1990s to the present. This review begins by exploring the role of microbiota in modulating host health and disease. It then examines how disturbances in maternal microbiota can affect the offspring's immune system. The analysis continues by investigating the interplay between stress and dysbiosis, focusing on how prenatal maternal stress influences both maternal and offspring microbiota and its implications for susceptibility to depression. The review also considers the impact of ethanol consumption on gut dysbiosis, with an emphasis on the effects of prenatal ethanol exposure on both maternal and offspring microbiota. Finally, it is suggested that maternal gut microbiota dysbiosis may be significantly exacerbated by the combined effects of stress and ethanol exposure, leading to immune system dysfunction and chronic inflammation, which could increase the risk of depression in the offspring. These interactions underscore the potential for novel mental health interventions that address the gut-brain axis, especially in relation to maternal and offspring health.

Cutting-Edge iPSC-Based Approaches in Studying Host-Microbe Interactions in Neuropsychiatric Disorders.

Gut microbiota (GM), together with its metabolites (such as SCFA, tryptophan, dopamine, GABA, etc.), plays an important role in the functioning of the central nervous system. Various neurological and psychiatric disorders are associated with changes in the composition of GM and their metabolites, which puts them in the foreground as a potential adjuvant therapy. However, the molecular mechanisms behind this relationship are not clear enough. Therefore, before considering beneficial microbes and/or their metabolites as potential therapeutics for brain disorders, the mechanisms underlying microbiota-host interactions must be identified and characterized in detail. In this review, we summarize the current knowledge of GM alterations observed in prevalent neurological and psychiatric disorders, multiple sclerosis, major depressive disorder, Alzheimer's disease, and autism spectrum disorders, together with experimental evidence of their potential to improve patients' quality of life. We further discuss the main obstacles in the study of GM-host interactions and describe the state-of-the-art solution and trends in this field, namely "culturomics" which enables the culture and identification of novel bacteria that inhabit the human gut, and models of the gut and blood-brain barrier as well as the gut-brain axis based on induced pluripotent stem cells (iPSCs) and iPSC derivatives, thus pursuing a personalized medicine agenda for neuropsychiatric disorders.

Testing a Conceptual Model of Early Adversity, Neural Function, and Psychopathology: Protocol for a Retrospective Observational Cohort Study.

BACKGROUND: Early adversity, broadly defined as a set of negative exposures during childhood, is extremely common and increases risk for psychopathology across the life span. Previous research suggests that separate dimensions of adversity increase risk through developmental plasticity mechanisms shaping unique neurobiological pathways. Specifically, research suggests that deprivation is associated with deficits in higher order cognition, while threat is associated with atypicality in fear learning and emotion dysregulation. However, most of this research has been conducted in adolescent and adult samples, long after exposure to adversity occurs and far from periods of peak developmental plasticity. OBJECTIVE: The Wellness Health and Life Experiences (WHALE) study examines the neurobiological and behavioral mechanisms by which deprivation, threat, and unpredictability increase risk for psychopathology in early childhood (age 4-7 years) directly following periods of peak developmental plasticity. The objective of this study is to describe the study rationale and aims, the research design and procedures, and the analytical plan to test the study hypotheses. METHODS: This is a retrospective cohort study that examines associations between exposure to deprivation and threat and their hypothesized neurobiological mechanisms, how these neurobiological mechanisms link early adversity and psychopathology, and associations between unpredictability, reward learning, and psychopathology. The sample was a convenience sample of children (aged 4-7 years) and their families, identified through flyers, email blasts to listserves, school-based advertising, and involvement in community events. Data were collected during a home visit, a subsequent laboratory visit, and a final neuroimaging visit. Planned analyses include linear regression, path analyses, and functional magnetic resonance imaging analyses to explore the role of neural function in the association between early adversity and psychopathology. RESULTS: Participants (N=301) have been recruited into the study, and data collection has commenced. The expected results will be available in 2024. CONCLUSIONS: The findings of this study will help elucidate the neurobiological mechanisms by which early adversity increases risk for psychopathology in early childhood. This study represents the earliest test of an influential theory of biological embedding of early adversity. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): DERR1-10.2196/59636.

Evaluating the distinct effects of body mass index at childhood and adulthood on adult major psychiatric disorders.

Children with high body mass index (BMI) are at heightened risk of developing health issues in adulthood, yet the causality between childhood BMI and adult psychiatric disorders remains unclear. Using a life course Mendelian randomization (MR) framework, we investigated the causal effects of childhood and adulthood BMI on adult psychiatric disorders, including Alzheimer's disease, anxiety, major depressive disorder, obsessive-compulsive disorder (OCD), and schizophrenia, using data from the Psychiatric Genomics Consortium and FinnGen study. Childhood BMI was significantly associated with an increased risk of schizophrenia, while adulthood BMI was associated with a decreased risk of OCD and schizophrenia. Multivariable MR analyses indicated a direct causal effect of childhood BMI on schizophrenia, independent of adulthood BMI and lifestyle factors. No evidence of causal associations was found between childhood BMI and other psychiatric outcomes. The sensitivity analyses yielded broadly consistent findings. These findings highlight the critical importance of early-life interventions to mitigate the long-term consequences of childhood adiposity.

Experiences and Challenges Updating a Living Evidence-Based Review of Randomized Controlled Trials on Mental Health and Behavioral Disorders in Individuals With Moderate to Severe Traumatic Brain Injury.

OBJECTIVE: To describe experiences and challenges when updating a living evidence-based review database of randomized controlled trials (RCTs) on mental health and behavioral disorders in moderate to severe traumatic brain injury (MSTBI). METHOD: This commentary derives from our experience developing an extensive database of RCTs on MSTBI that has been conceptualized as a living evidence-based review. Our working group focused on mental health and behavior RCTs and reflected upon their experiences and challenges using the living systematic approach. We discuss challenges associated with metrics of study quality, injury etiology and severity, time post-injury, country of origin, and variability in outcome measures. RESULTS: RCTs were conducted almost solely in high income countries, with smaller sample sizes, and most conducted in the chronic phase post-TBI. Issues related to lack of transparency, unclear and incomplete reporting of injury severity, etiology, and time post-injury remain a concern and can lead to challenges associated with interpretation of results, validity, and reliability of the data. There was significant heterogeneity regarding the use of outcome measures and constructs, underscoring the need for standardization. CONCLUSION: Lack of standardization and incomplete reporting of injury characteristics makes it difficult to compare data between RCTs of MSTBI, perform meta-analyses, and generate evidence-based clinical recommendations.

Metabolic Insights into Neuropsychiatric Illnesses and Ketogenic Therapies: A Transcriptomic View.

The disruption of brain energy metabolism, leading to alterations in synaptic signaling, neural circuitry, and neuroplasticity, has been implicated in severe mental illnesses such as schizophrenia, bipolar disorder, and major depressive disorder. The therapeutic potential of ketogenic interventions in these disorders suggests a link between metabolic disturbances and disease pathology; however, the precise mechanisms underlying these metabolic disturbances, and the therapeutic effects of metabolic ketogenic therapy, remain poorly understood. In this study, we conducted an in silico analysis of transcriptomic data to investigate perturbations in metabolic pathways in the brain across severe mental illnesses via gene expression profiling. We also examined dysregulation of the same pathways in rodent or cell culture models of ketosis, comparing these expression profiles to those observed in the disease states. Our analysis revealed significant perturbations across all metabolic pathways, with the greatest perturbations in glycolysis, the tricarboxylic acid (TCA) cycle, and the electron transport chain (ETC) across all three disorders. Additionally, we observed some discordant gene expression patterns between disease states and ketogenic intervention studies, suggesting a potential role for ketone bodies in modulating pathogenic metabolic changes. Our findings highlight the importance of understanding metabolic dysregulation in severe mental illnesses and the potential therapeutic benefits of ketogenic interventions in restoring metabolic homeostasis. This study provides insights into the complex relationship between metabolism and neuropsychiatric disorders and lays the foundation for further experimental investigations aimed at appreciating the implications of the present transcriptomic findings as well as developing targeted therapeutic strategies.

[Mental disorders from climate and environmental changes using the example of dermatology]. / Psychische Folgen von Klima- und Umweltveränderungen am Beispiel der Dermatologie.

BACKGROUND: Global climate and environmental changes impose a significant impact on human health by increasing prevalences of chronic and acute skin diseases. Climate-associated environmental changes can also trigger or intensify mental illnesses independently of a skin disease. AIM: Discussion of the effects of the climate and environmental changes on dermatological diseases applying the biopsychosocial model. MATERIALS AND METHODS: A selective literature search in the PubMed database and other sources was conducted. RESULTS: The biopsychosocial model considers complex interactions between biological, psychological, and social factors. In view of the consequences of climate and environmental changes, an extension of the model is proposed for the first time in order to address new challenges. The modified presentation supports the understanding of the dynamics and underscores that in dermatological care not only direct health effects of climate and environmental changes have to be dealt with, but also with an increasing number of mental illnesses, which in turn are to be regarded as direct and indirect health effects. CONCLUSION: Coping with the predicted increase in the burden of disease and the decline in the available labor force associated with demographic change poses a major challenge. In order to maintain the functionality of the healthcare system, the prompt implementation of resource-efficient, sustainable measures in all areas of society is essential. The integrative consideration of dermatological and psychological complaints in the context of climate and environmental changes requires the adaptation of content for the education, training, and continuing education of specialists.

The Influence of Cecal Microbiota Transplantation on Chicken Injurious Behavior: Perspective in Human Neuropsychiatric Research.

Numerous studies have evidenced that neuropsychiatric disorders (mental illness and emotional disturbances) with aggression (or violence) pose a significant challenge to public health and contribute to a substantial economic burden worldwide. Especially, social disorganization (or social inequality) associated with childhood adversity has long-lasting effects on mental health, increasing the risk of developing neuropsychiatric disorders. Intestinal bacteria, functionally as an endocrine organ and a second brain, release various immunomodulators and bioactive compounds directly or indirectly regulating a host's physiological and behavioral homeostasis. Under various social challenges, stress-induced dysbiosis increases gut permeability causes serial reactions: releasing neurotoxic compounds, leading to neuroinflammation and neuronal injury, and eventually neuropsychiatric disorders associated with aggressive, violent, or impulsive behavior in humans and various animals via a complex bidirectional communication of the microbiota-gut-brain (MGB) axis. The dysregulation of the MGB axis has also been recognized as one of the reasons for the prevalence of social stress-induced injurious behaviors (feather pecking, aggression, and cannibalistic pecking) in chickens. However, existing knowledge of preventing and treating these disorders in both humans and chickens is not well understood. In previous studies, we developed a non-mammal model in an abnormal behavioral investigation by rationalizing the effects of gut microbiota on injurious behaviors in chickens. Based on our earlier success, the perspective article outlines the possibility of reducing stress-induced injurious behaviors in chickens through modifying gut microbiota via cecal microbiota transplantation, with the potential for providing a biotherapeutic rationale for preventing injurious behaviors among individuals with mental disorders via restoring gut microbiota diversity and function.

A comprehensive assessment of the association between common drugs and psychiatric disorders using Mendelian randomization and real-world pharmacovigilance database.

BACKGROUND: Medications prescribed for chronic diseases can lead to short-term neuropsychiatric symptoms, but their long-term effects on brain structures and psychiatric conditions remain unclear. METHODS: We comprehensively analyzed the FDA Adverse Event Reporting System database and conducted drug target Mendelian Randomization (MR) studies on six categories of common drugs, 477 brain imaging-derived phenotypes (IDPs) and eight psychiatric disorders. Genetic instruments were extracted from expression quantitative trait loci (eQTLs) in blood, brain, and other target tissues, protein quantitative trait loci (pQTLs) in blood, and genome-wide association studies (GWAS) of hemoglobin and cholesterol. Summary statistics for brain IDPs, psychiatric disorders, and gut microbiome were obtained from the BIG40, Psychiatric Genomics Consortium, and MiBioGen. A two-step MR and mediation analysis were employed to screen possible mediators of drug-IDP effects from 119 gut microbiota genera and identify their mediation proportions. FINDINGS: Among 19 drug classes, six drugs were found to be associated with higher risks of psychiatric adverse events, while 11 drugs were associated with higher risks of gastrointestinal adverse events in the FAERS analysis. We identified ten drug-psychiatric disorder associations, 202 drug-IDP associations, 16 drug-microbiota associations, and four drug-microbiota-IDP causal links. For example, PPARG activation mediated HbA1c reduction caused a higher risk of bipolar disorder (BD) II. Genetically proxied GLP-1R agonists were significantly associated with an increase in the volume of the CA3-head of the right hippocampus and the area of the left precuneus cortex, both of which have been shown to correlate with cognition in previous studies. INTERPRETATION: Common drugs may affect brain structure and risk of psychiatric disorder. Oral medications in particular may exert some of these effects by influencing gut microbiota. This study calls for greater attention to be paid to the neuropsychiatric adverse effects of drugs and encourages drug repurposing. FUNDING: National Natural Science Foundation of China (grant No. 82330035, 82130043, 82172685, and 82001223), National Natural Science Foundation of Hunan Province (grant No. 2021SK1010), and the Science Foundation for Distinguished Young Scholars of Changsha (grant No. kq2209006).

Self-perceived quality of life, cognitive and behavioural impairment in amyotrophic lateral sclerosis.

BACKGROUND: Self-perceived quality of life (QoL) is important in amyotrophic lateral sclerosis (ALS). Although caregiver burden and strain have been related to cognitive and behavioural impairment, there has been no comprehensive research looking at these impairments and how they may influence self-perceived QoL subdomains. AIMS: To explore how cognitive and behavioural impairment are related to different areas of self-perceived QoL using disease-specific measures. METHODS: This was a quantitative, cross-sectional, observational cohort study, utilising existing specialist ALS clinic data. Clinical and demographic variables were available as well as multidimensional measures, ALS-specific QoL Short Form (ALSsQoL-SF) results and the data from the Edinburgh Cognitive and Behavioural ALS Screen (ECAS). Group comparison and regression analyses were performed. RESULTS: Data from 121 participants with ALS were analysed. 61.2% (N = 74) had either cognitive and/or behavioural impairment, with 28.9% (N = 35) with cognitive impairment (ALSci), 14.1% (N = 17) with behavioural impairment (ALSbi) and 18.2% (N = 22) with both (ALScbi). 38.8% (N = 47) were classified as having no impairments (ALSni). Those with ALSbi had significantly lower QoL in the domains of negative emotions and the interaction with people and the environment compared to those with ALSci and ALSni (ps < 0.05). Further, those with ALScbi had significantly lower QoL in the intimacy domains than those with ALSci and ALSni (ps < 0.05). Regression analysis showed specific cognitive and behavioural (inclusive of psychosis) predictors associated with specific QoL subdomains. CONCLUSIONS: Behavioural impairments effect QoL in specific subdomains, namely relating to internalising (negative emotions) and externalising (interaction with people and the environment subdomains, intimacy).

Isolated Psychiatric Symptoms in Children With Anti-N-Methyl-d Aspartate Receptor Encephalitis.

BACKGROUND: Isolated psychiatric symptoms can be the initial symptom of pediatric anti-N-methyl-d-aspartate (NMDA) receptor autoimmune encephalitis (pNMDARE). Here we report on the prevalence of isolated psychiatric symptoms in pNMDARE. We also assess whether initial neurodiagnostic tests (brain magnetic resonance imaging [MRI], electroencephalography [EEG], and/or cerebrospinal fluid [CSF] white blood cell count) are abnormal in children with isolated psychiatric symptoms and pNMDARE. METHODS: This multicenter retrospective cohort study from CONNECT (Conquering Neuroinflammation and Epilepsies Consortium) from 14 institutions included children under age 18 years who were diagnosed with pNMDARE. Descriptive statistics using means, medians, and comparisons for continuous versus discrete data was performed. RESULTS: Of 249 children included, 12 (5%) had only psychiatric symptoms without other typical clinical features of autoimmune encephalitis at presentation. All but one (11 of 12 = 92%) had at least one abnormal finding on initial ancillary testing: eight of 12 (67%) had an abnormal EEG, six of 12 (50%) had an abnormal MRI, and five of 12 (42%) demonstrated CSF pleocytosis. The single patient with a normal MRI, EEG, and CSF profile had low positive CSF NMDA antibody (titer of 1:1), and symptoms improved without immunotherapy. CONCLUSIONS: Isolated first-episode psychiatric symptoms in pNMDARE are uncommon, and the majority of children will exhibit additional neurodiagnostic abnormalities. Delaying immunotherapy in a child with isolated psychiatric symptoms and normal neurodiagnostic testing may be warranted while awaiting confirmatory antibody testing.

Viral infections in etiology of mental disorders: a broad analysis of cytokine profile similarities - a narrative review.

The recent pandemic caused by the SARS-CoV-2 virus and the associated mental health complications have renewed scholarly interest in the relationship between viral infections and the development of mental illnesses, a topic that was extensively discussed in the previous century in the context of other viruses, such as influenza. The most probable and analyzable mechanism through which viruses influence the onset of mental illnesses is the inflammation they provoke. Both infections and mental illnesses share a common characteristic: an imbalance in inflammatory factors. In this study, we sought to analyze and compare cytokine profiles in individuals infected with viruses and those suffering from mental illnesses. The objective was to determine whether specific viral diseases can increase the risk of specific mental disorders and whether this risk can be predicted based on the cytokine profile of the viral disease. To this end, we reviewed existing literature, constructed cytokine profiles for various mental and viral diseases, and conducted comparative analyses. The collected data indicate that the risk of developing a specific mental illness cannot be determined solely based on cytokine profiles. However, it was observed that the combination of IL-8 and IL-10 is frequently associated with psychotic symptoms. Therefore, to assess the risk of mental disorders in infected patients, it is imperative to consider the type of virus, the mental complications commonly associated with it, the predominant cytokines to evaluate the risk of psychotic symptoms, and additional patient-specific risk factors.

Predictors of Psychiatric Complications in Patients with Pancreatic Cancer: A Retrospective Cohort Study.

BACKGROUND: The relevant survey has shown a high incidence of psychiatric complications in patients with pancreatic cancer. While some studies have explored the factors influencing psychological complications in pancreatic cancer patients, some factors validated in other populations have not been confirmed in the pancreatic cancer population. This study aims to explore the predictors of psychiatric complications in patients with pancreatic cancer. METHODS: Patients with pancreatic cancer admitted to Yueqing People's Hospital Affiliated to Wenzhou Medical University, from January 2021 to January 2022 were retrospectively analyzed. The structured clinical interview (SCID-I) based on Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) was used by nurses to assess the incidence of psychiatric complications during hospitalization (baseline) and 3 months after the start of treatment. Binary logistic regression was used to identify predictors of psychiatric complications. RESULTS: 80 patients were enrolled in this study and 8 patients were diagnosed with psychiatric complications at base line. Among the rest 72 patients, 8 patients (11.11%) had new-onset psychiatric complications at 3-month follow-up. Gender (Odds Ratio (OR) = 1.674, p = 0.019), monthly income (OR = 1.735, p = 0.023) and sadness (M.D. Anderson Symptom Inventory (MDASI)) (OR = 1.804, p = 0.001) were all predictors for psychiatric complications in patients with pancreatic cancer. CONCLUSIONS: Gender, monthly income and MDASI score are predictors of psychiatric complications in patients with pancreatic cancer.

Estimation of Attributable Risk and Direct Medical and Non-Medical Costs of Major Mental Disorders Associated With Air Pollution Exposures Among Children and Adolescents in the Republic of Korea, 2011-2019.

BACKGROUND: Recent studies have reported the burden of attention deficit hyperactivity disorder [ADHD], autism spectrum disorder [ASD], and depressive disorder. Also, there is mounting evidence on the effects of environmental factors, such as ambient air pollution, on these disorders among children and adolescents. However, few studies have evaluated the burden of mental disorders attributable to air pollution exposure in children and adolescents. METHODS: We estimated the risk ratios of major mental disorders (ADHD, ASD, and depressive disorder) associated with air pollutants among children and adolescents using time-series data (2011-2019) obtained from a nationwide air pollution monitoring network and healthcare utilization claims data in the Republic of Korea. Based on the estimated risk ratios, we determined the population attributable fraction (PAF) and calculated the medical costs of major mental disorders attributable to air pollution. RESULTS: A total of 33,598 patients were diagnosed with major mental disorders during 9 years. The PAFs for all the major mental disorders were estimated at 6.9% (particulate matter < 10 µm [PM10]), 3.7% (PM2.5), and 2.2% (sulfur dioxide [SO2]). The PAF of PM10 was highest for depressive disorder (9.2%), followed by ASD (8.4%) and ADHD (5.2%). The direct medical costs of all major mental disorders attributable to PM10 and SO2 decreased during the study period. CONCLUSION: This study assessed the burden of major mental disorders attributable to air pollution exposure in children and adolescents. We found that PM10, PM2.5, and SO2 attributed 7%, 4%, and 2% respectively, to the risk of major mental disorders among children and adolescents.

The neurocognitive and neuropsychiatric manifestations of Susac syndrome: a brief review of the literature and future directions.

Encephalopathy is part of the clinical triad of Susac syndrome, but a detailed understanding of the neurocognitive and neuropsychiatric profile of this condition is lacking. Existing literature indicates that cognitive deficits range in severity from subtle to profound. Executive function and short-term recall are affected frequently. Psychiatric manifestations may be absent or may include anxiety, mood disorders or psychosis. If psychiatric phenomena develop during the disease course, it can be hard to disentangle whether symptoms directly relate to the pathology of Susac syndrome or are secondary to treatment-related side effects. In this article, we review what is known about the cognitive and psychiatric morbidity of Susac syndrome and identify areas where knowledge is deficient. Importantly, we also provide a framework for future research, arguing that better phenotyping, understanding of pathophysiology, evaluation of treatments on cognitive and psychiatric outcomes, and longitudinal data capture are vital to improving patient outcomes.

Introducing the Role of Genotoxicity in Neurodegenerative Diseases and Neuropsychiatric Disorders.

Decades of research have identified genetic and environmental factors involved in age-related neurodegenerative diseases and, to a lesser extent, neuropsychiatric disorders. Genomic instability, i.e., the loss of genome integrity, is a common feature among both neurodegenerative (mayo-trophic lateral sclerosis, Parkinson's disease, Alzheimer's disease) and psychiatric (schizophrenia, autism, bipolar depression) disorders. Genomic instability is associated with the accumulation of persistent DNA damage and the activation of DNA damage response (DDR) pathways, as well as pathologic neuronal cell loss or senescence. Typically, DDR signaling ensures that genomic and proteomic homeostasis are maintained in both dividing cells, including neural progenitors, and post-mitotic neurons. However, dysregulation of these protective responses, in part due to aging or environmental insults, contributes to the progressive development of neurodegenerative and/or psychiatric disorders. In this Special Issue, we introduce and highlight the overlap between neurodegenerative diseases and neuropsychiatric disorders, as well as the emerging clinical, genomic, and molecular evidence for the contributions of DNA damage and aberrant DNA repair. Our goal is to illuminate the importance of this subject to uncover possible treatment and prevention strategies for relevant devastating brain diseases.