Explore the vast range of titles available.

Obesity is associated with an increased risk of several neurological and psychiatric diseases, but few studies report the contribution of biological features in the occurrence of mood disorders in obese patients. The aim of the study is to evaluate the potential links between serum metabolomics and gut microbiome, and mood disturbances in a cohort of obese patients. Psychological, biological characteristics and nutritional habits were evaluated in 94 obese subjects from the Food4Gut study stratified according to their mood score assessed by the Positive and Negative Affect Schedule (PANAS). The fecal gut microbiota and plasma non-targeted metabolomics were analysed. Obese subjects with increased negative mood display elevated levels of Coprococcus as well as decreased levels of Sutterella and Lactobacillus. Serum metabolite profile analysis reveals in these subjects altered levels of several amino acid-derived metabolites, such as an increased level of L-histidine and a decreased in phenylacetylglutamine, linked to altered gut microbiota composition and function rather than to differences in dietary amino acid intake. Regarding clinical profile, we did not observe any differences between both groups. Our results reveal new microbiota-derived metabolites that characterize the alterations of mood in obese subjects, thereby allowing to propose new targets to tackle mood disturbances in this context. Food4gut, clinicaltrial.gov: NCT03852069.

The behavioral syndrome resulting from damage to the ventromedial prefrontal (VM) region presents major challenges for clinical assessment and management, stemming from the absence of reliable neurologic or psychometric markers, coupled with often debilitating impairments of decision-making and behavior regulation. Damage to this region disrupts neural circuitry critical for emotion, which in turn may contribute to impairments in real-world competencies. Here we present findings from patients with focal lesions in the VM region acquired either in childhood or adulthood, and show that there is a relationship between emotional dysfunction and impairments in real-world behavioral competencies. Emotion was rated by participants' relatives on dimensions including frustration tolerance, lability, anxiety, and blunted affect. Real-world competencies were rated by the relatives on dimensions including judgment, planning, and initiation, and were evaluated by clinician ratings in areas including social, financial, and occupational function. VM damage resulted in severe disruption of emotion, and this emotional dysfunction accounted for a significant portion of impaired real-world competencies. The long-term impairments associated with childhood-onset lesions were at least as severe as those resulting from adult-onset damage. Greater focus on the contribution of emotional dysfunction to the real-world competencies of patients with damage in the VM region may sharpen their neuropsychological assessment and facilitate rehabilitation efforts. (JINS, 2006, 12, 224–235.)

Patients with glioma present with complex palliative care needs throughout their disease trajectory. The life-limiting nature of gliomas and the presence of specific symptoms related to neurological deterioration necessitate an appropriate and early palliative care approach. The multidisciplinary palliative care task force of the European Association of Neuro-Oncology did a systematic review of the available scientific literature to formulate the best possible evidence-based recommendations for the palliative care of adult patients with glioma, with the aim to reduce symptom burden and improve the quality of life of patients and their caregivers, particularly in the end-of-life phase. When recommendations could not be made because of the scarcity of evidence, the task force either used evidence from studies of patients with systemic cancer or formulated expert opinion. Areas of palliative care that currently lack evidence and thus deserve attention for further research are fatigue, disorders of behaviour and mood, interventions for the needs of caregivers, and timing of advance care planning.

The United Nations warned of COVID-19-related mental health crisis; however, it is unknown whether there is an increase in the prevalence of mental disorders as existing studies lack a reliable baseline analysis or they did not use a diagnostic measure. We aimed to analyse trends in the prevalence of mental disorders prior to and during the COVID-19 pandemic. We analysed data from repeated cross-sectional surveys on a representative sample of non-institutionalised Czech adults (18+ years) from both November 2017 (n = 3306; 54% females) and May 2020 (n = 3021; 52% females). We used Mini International Neuropsychiatric Interview (MINI) as the main screening instrument. We calculated descriptive statistics and compared the prevalence of current mood and anxiety disorders, suicide risk and alcohol-related disorders at baseline and right after the first peak of COVID-19 when related lockdown was still in place in CZ. In addition, using logistic regression, we assessed the association between COVID-19-related worries and the presence of mental disorders. The prevalence of those experiencing symptoms of at least one current mental disorder rose from a baseline of 20.02 (95% CI = 18.64; 21.39) in 2017 to 29.63 (95% CI = 27.9; 31.37) in 2020 during the COVID-19 pandemic. The prevalence of both major depressive disorder (3.96, 95% CI = 3.28; 4.62 v. 11.77, 95% CI = 10.56; 12.99); and suicide risk (3.88, 95% CI = 3.21; 4.52 v. 11.88, 95% CI = 10.64; 13.07) tripled and current anxiety disorders almost doubled (7.79, 95% CI = 6.87; 8.7 v. 12.84, 95% CI = 11.6; 14.05). The prevalence of alcohol use disorders in 2020 was approximately the same as in 2017 (10.84, 95% CI = 9.78; 11.89 v. 9.88, 95% CI = 8.74; 10.98); however, there was a significant increase in weekly binge drinking behaviours (4.07% v. 6.39%). Strong worries about both, health or economic consequences of COVID-19, were associated with an increased odds of having a mental disorder (1.63, 95% CI = 1.4; 1.89 and 1.42, 95% CI = 1.23; 1.63 respectively). This study provides evidence matching concerns that COVID-19-related mental health problems pose a major threat to populations, particularly considering the barriers in service provision posed during lockdown. This finding emphasises an urgent need to scale up mental health promotion and prevention globally.

Key Points Individuals with rheumatoid arthritis (RA) demonstrate an increased prevalence of mood disorders compared with the general population, but a decreased prevalence of schizophrenia, probably due to alterations in inflammatory processes Several mechanisms underlie the relationship between RA and mental health comorbidities: cognitive, behavioural and affective responses, inflammatory processes, and fatigue Social factors have important implications in psychological reactions to RA, and could also be involved in pain processing and RA disease activity Neural reward-processing deficiencies are an emerging area of inquiry in understanding the relationship between pain and psychological states that warrants additional attention in patients with RA Psychological treatments that increase active coping strategies, ameliorate affective distress, bolster self-efficacy, and increase supportive social relationships could improve treatment outcomes in patients with RA Mental health-related comorbidities can negatively affect the quality of life of patients with rheumatoid arthritis. In this Review, the authors discuss how psychological manifestations interact with disease processes, new insights into neurological processing in chronic pain, and psychological interventions. In addition to recurrent pain, fatigue, and increased rates of physical disability, individuals with rheumatoid arthritis (RA) have an increased prevalence of some mental health disorders, particularly those involving affective or mood disturbances. This narrative Review provides an overview of mental health comorbidities in RA, and discusses how these comorbidities interact with disease processes, including dysregulation of inflammatory responses, prolonged difficulties with pain and fatigue, and the development of cognitive and behavioural responses that could exacerbate the physical and psychological difficulties associated with RA. This article describes how the social context of individuals with RA affects both their coping strategies and their psychological responses to the disease, and can also impair responses to treatment through disruption of patient-physician relationships and treatment adherence. Evidence from the literature on chronic pain suggests that the resulting alterations in neural pathways of reward processing could yield new insights into the connections between disease processes in RA and psychological distress. Finally, the role of psychological interventions in the effective and comprehensive treatment of RA is discussed.

The consumption of caffeine (an adenosine receptor antagonist) correlates inversely with depression and memory deterioration, and adenosine A2A receptor (A2AR) antagonists emerge as candidate therapeutic targets because they control aberrant synaptic plasticity and afford neuroprotection. Therefore we tested the ability of A2AR to control the behavioral, electrophysiological, and neurochemical modifications caused by chronic unpredictable stress (CUS), which alters hippocampal circuits, dampens mood and memory performance, and enhances susceptibility to depression. CUS for 3 wk in adult mice induced anxiogenic and helpless-like behavior and decreased memory performance. These behavioral changes were accompanied by synaptic alterations, typified by a decrease in synaptic plasticity and a reduced density of synaptic proteins (synaptosomal-associated protein 25, syntaxin, and vesicular glutamate transporter type 1), together with an increased density of A2AR in glutamatergic terminals in the hippocampus. Except for anxiety, for which results were mixed, CUS-induced behavioral and synaptic alterations were prevented by (i) caffeine (1 g/L in the drinking water, starting 3 wk before and continued throughout CUS); (ii) the selective A2AR antagonist KW6002 (3 mg/kg, p.o.); (iii) global A2AR deletion; and (iv) selective A2AR deletion in forebrain neurons. Notably, A2AR blockade was not only prophylactic but also therapeutically efficacious, because a 3-wk treatment with the A2AR antagonist SCH58261 (0.1 mg/kg, i.p.) reversed the mood and synaptic dysfunction caused by CUS. These results herald a key role for synaptic A2AR in the control of chronic stress-induced modifications and suggest A2AR as candidate targets to alleviate the consequences of chronic stress on brain function.

Outcomes after acute respiratory distress syndrome (ARDS) are similar to those of other survivors of critical illness and largely affect the nerve, muscle, and central nervous system but also include a constellation of varied physical devastations ranging from contractures and frozen joints to tooth loss and cosmesis. Compromised quality of life is related to a spectrum of impairment of physical, social, emotional, and neurocognitive function and to a much lesser extent discrete pulmonary disability. Intensive care unit-acquired weakness (ICUAW) is ubiquitous and includes contributions from both critical illness polyneuropathy and myopathy, and recovery from these lesions may be incomplete at 5 years after ICU discharge. Cognitive impairment in ARDS survivors ranges from 70 to 100 % at hospital discharge, 46 to 80 % at 1 year, and 20 % at 5 years, and mood disorders including depression and post-traumatic stress disorder (PTSD) are also sustained and prevalent. Robust multidisciplinary and longitudinal interventions that improve these outcomes are still uncertain and data in our literature are conflicting. Studies are needed in family members of ARDS survivors to better understand long-term outcomes of the post-ICU family syndrome and to evaluate how it affects patient recovery.

Major depressive disorder (MDD) and other mood disorders remain difficult to effectively treat, and innovative interventions and therapeutic targets are needed. Psychological stressors and inappropriate inflammation increase the risk and severity of mood disorders; however, only recently have the importance of sterile inflammatory processes in this effect been revealed. This review will introduce the reader to pathogen vs sterile inflammation, inflammatory receptor-ligand interactions, microbial-associated molecular patterns (MAMPs), pathogen-associated molecular patterns (PAMPs), danger-associated molecular patterns (DAMPs), and the more recent discovery of the role of the inflammasome in peripheral and central nervous system cytokine/chemokine inflammatory responses. The review will focus on current preclinical and clinical evidence that sterile inflammation and inflammasome-dependent signaling may contribute to mood disorders. By understanding these inflammatory signaling processes, new approaches for quieting chronic or inappropriate inflammatory states may be revealed and this could serve as novel pharmacological targets for the treatment of mood disorders.

Stress-related variation in the intrauterine milieu may impact brain development and emergent function, with long-term implications in terms of susceptibility for affective disorders. Studies in animals suggest limbic regions in the developing brain are particularly sensitive to exposure to the stress hormone cortisol. However, the nature, magnitude, and time course of these effects have not yet been adequately characterized in humans. A prospective, longitudinal study was conducted in 65 normal, healthy mother–child dyads to examine the association of maternal cortisol in early, mid-, and late gestation with subsequent measures at approximately 7 y age of child amygdala and hippocampus volume and affective problems. After accounting for the effects of potential confounding pre- and postnatal factors, higher maternal cortisol levels in earlier but not later gestation was associated with a larger right amygdala volume in girls (a 1 SD increase in cortisol was associated with a 6.4% increase in right amygdala volume), but not in boys. Moreover, higher maternal cortisol levels in early gestation was associated with more affective problems in girls, and this association was mediated, in part, by amygdala volume. No association between maternal cortisol in pregnancy and child hippocampus volume was observed in either sex. The current findings represent, to the best of our knowledge, the first report linking maternal stress hormone levels in human pregnancy with subsequent child amygdala volume and affect. The results underscore the importance of the intrauterine environment and suggest the origins of neuropsychiatric disorders may have their foundations early in life.

Globally, more than 20% of women of reproductive age are currently estimated to be obese. Children born to obese mothers are at higher risk of developing obesity, coronary heart disease, diabetes, stroke, and asthma in adulthood. Increasing clinical and experimental evidence suggests that maternal obesity also affects the health and function of the offspring brain across the lifespan. This review summarizes the current findings from human and animal studies that detail the impact of maternal obesity on aspects of learning, memory, motivation, affective disorders, attention-deficit hyperactivity disorder, autism spectrum disorders, and neurodegeneration in the offspring. Epigenetic mechanisms that may contribute to this mother–child interaction are also discussed.