Neuropsychiatric Symptoms Research Articles

Chronic Hepatitis D Virus Infection and Its Treatment: A Narrative Review

More than 12 million individuals worldwide are chronically infected with the hepatitis D virus (HDV). HDV infection is the most severe form of viral hepatitis since it requires hepatitis B virus co-infection and accelerates progression to cirrhosis and hepatocellular carcinoma. Therefore, treatment modalities to slow the progression of the disease are essential but not yet available. In addition, no antiviral treatment to date has been shown to reliably eradicate HDV. Pegylated interferon (PEG-IFN) is the only universally used treatment to suppress HDV RNA replication and improve liver inflammation and fibrosis. This treatment can be completed in 12–18 months, but cure rates remain low, and success does not reliably increase with the addition of a nucleos(t)ide analog. PEG-IFN therapy is also limited by poor tolerability and multiple adverse effects, including neutropenia, thrombocytopenia, and neuropsychiatric symptoms. Newer antiviral therapies in development target unique aspects of HDV viral replication and show promising results in combination with PEG-IFN for long-term HDV RNA suppression. These newer antiviral therapies include buleviritide (which blocks HDV entry), lonafarnib (which prevents HDV assembly), and REP-2139 (which prevents HDV export). In this manuscript, we discuss the characteristics of HDV infection and review the new antiviral therapies approved for treatment and those under investigation.

Different physical exercise in the treatment of Alzheimer's disease.

Alzheimer's disease (AD) is rapidly becoming one of the most expensive, burdening, and deadly diseases of this century. Up to now, there is still a lack of pharmacotherapy with substantial efficacy, and physical exercise is a promising and low-cost way to aid in delaying the process of AD. The aim of this review is to summarise the efficacy of different physical exercise approaches and doses in the management of AD, including aerobic exercise, resistance exercise and multicomponent exercise. A literature search using MeSH terms for each topic is undertaken using PubMed and the Web of Science Core Collection database, supplemented by hand searching for additional references. Retrieved articles were reviewed, synthesised, and summarised. This review shows that aerobic exercise has been almost unanimously recognised for the improvement of cognition, neuropsychiatric symptoms and activities of daily living. Resistance exercise also shows a good prospect in the above aspects and has a unique advantage in enhancing muscle strength, while multicomponent physical activity does not seen to significantly improve cognitive function. Each type of exercise has a dose effect, but for individuals with AD, the most appropriate exercise dose is still controversial.

Deciphering the effects of STN DBS on neuropsychiatric fluctuations in Parkinson’s disease

The impact of subthalamic nucleus (STN) deep brain stimulation (DBS) on neuropsychiatric fluctuations in Parkinson´s disease (PD) remains unclear. The Neuropsychiatric Fluctuations Scale (NFS) can help to fill this gap, directly measuring fluctuations between the OFF- and ON-medication conditions. The NFS provides NFS-plus (hyperdopaminergic) and NFS-minus (hypodopaminergic) sub-scores. Based on these, the NFS global scores express the overall magnitude of neuropsychiatric symptoms in both the OFF- and ON-medication states. The total fluctuation score (TFS) represents the difference between ON- vs. OFF-medication NFS global scores, thus assessing fluctuations amplitude. The NFS was used to evaluate changes in neuropsychiatric fluctuations between the OFF- and ON-medication conditions before and 1-year after bilateral STN-DBS in 45 PD patients (32 males; mean age, 61.3 ± 7.2 years; PD duration, 10.2 ± 3.0 years). After surgery, the amplitude of neuropsychiatric fluctuations was significantly reduced (p < 0.001), confirming the efficacy of STN-DBS on these symptoms.

The Impact of Caregiving on Informal Caregivers of People with Dementia: Family Functioning, Burden, and Burnout.

Caregiving is a complex occupation, with a significant impact for informal caregivers (IC). Stress-process models propose a framework that considers that this impact depends on primary and secondary stressors, but also on the IC situation appraisal. This work aimed to verify: whether being, or not, an IC of an individual with dementia influenced the relationship between family functioning and burnout; the association between neuropsychiatric symptoms of the individual with dementia and IC burnout and whether the IC burden and perceived family functioning had a mediating role in such relationship. This cross-sectional study investigated differences in family functioning and its association with burnout between IC and non-IC. For IC specifically, the study examined a mediation model to explore the possibility of neuropsychiatric symptoms indirectly affecting IC burnout through the impact on family functioning and burden. Measures included the Copenhagen Burnout Inventory, the McMaster Family Assessment Device, the Neuropsychiatric Inventory, and the Zarit Burden Interview. Results showed an association between poorer family function and high burnout, specifically in IC. They also showed that burden mediated the relationship between neuropsychiatric symptoms and burnout. The findings offer a significant contribution to the growing knowledge about the relationship between stressors associated with informal caregiving in dementia context, such as neuropsychiatric symptoms and its outcomes, like burnout.

Wilson’s disease: A Comprehensive Review of Genetics, Pathophysiology, Clinical Symptoms, Diagnostic Techniques and Current Treatment

Introduction: Wilson's disease (WD) is a genetic disease, inherited in an autosomal recessive manner, caused by a mutation in the ATP7B gene, which results in impaired excretion of copper in the bile. This causes the accumulation of copper in various tissues and organs, leading to their damage. The range and severity of symptoms are wide, so diagnosis is difficult and requires a high index of suspicion. The most common clinical symptoms are hepatic and neuropsychiatric symptoms. Diagnosis is based primarily on clinical suspicion, typical symptoms and reduced serum ceruloplasmin concentration. Treatment includes pharmacological therapies, and in some cases liver transplantation is necessary. Wilson's disease, if left untreated, inevitably leads to serious disability and death. Purpose of the work: This study aims to review and characterize the clinical and pathophysiological aspects of Wilson’s disease. Materials and methods: A comprehensive analysis of research papers available on PubMed, Google Scholar, Web of Science, Embase and Scopus was undertaken using the searchterms encompassing the following keywords: Wilson’s disease, Copper metabolism, Copper toxicity, ATP7B, Ceruloplasmin, Gene Mutation Results: Wilson's disease is a rare genetic disorder that can lead to severe disability and even death. For this reason, rapid diagnosis and appropriately selected and individualized treatment play a key role. Wilson's disease remains a major diagnostic challenge, but new techniques for its diagnosis, such as genotype analysis, mainly through sequencing, as well as newborn screening, may significantly improve patient prognosis in the future.

An overview of the pathophysiology of agitation in Alzheimer's dementia with a focus on neurotransmitters and circuits.

Alzheimer's dementia (AD) is a progressive, neurodegenerative disease often accompanied by neuropsychiatric symptoms that profoundly impact both patients and caregivers. Agitation is among the most prevalent and distressing of these symptoms and often requires treatment. Appropriate therapeutic interventions depend on understanding the biological basis of agitation and how it may be affected by treatment. This narrative review discusses a proposed pathophysiology of agitation in Alzheimer's dementia based on convergent evidence across research approaches. Available data indicate that agitation in Alzheimer's dementia is associated with an imbalance of activity between key prefrontal and subcortical brain regions. The monoamine neurotransmitter systems serve as key modulators of activity within these brain regions and circuits and are rendered abnormal in AD. Patients with AD who exhibited agitation symptoms during life have alterations in neurotransmitter nuclei and related systems when the brain is examined at autopsy. The authors present a model of agitation in Alzheimer's dementia in which noradrenergic hyperactivity along with serotonergic deficits and dysregulated striatal dopamine release contribute to agitated and aggressive behaviors.

The Impact of Behavioral and Psychological Symptoms of Dementia on Individual's Autonomy: a Scoping Review.

The purpose of this study was to identify, map, summarize, and clarify the existing literature on the effects of behavioral and psychological symptoms of dementia (BPSD) an individual's autonomy across all types of dementia diagnoses. The study aimed to determine whether there is a correlation between BPSD and a decrease in a person's autonomy, as this relationship is important for improving dementia care through effective interventions. To achieve this goal, a scoping review was conducted using the Joanna Briggs Institute's methodology for scoping reviews and the PRISMA extension for scoping reviews checklist. The inclusion criteria were: (i) population: participants with a clinical diagnosis of any type of dementia; (ii) concept: examining the relationship between one or more neuropsychiatric symptoms or BPSD and the individual's autonomy; (iii) context: the progress of any type and any stage of dementia. The database search yielded 74 records, of which 41 fully met the pre-established eligibility criteria. Most studies in this review focused on participants with Alzheimer's disease and analysed their functional abilities. Most studies in this review showed significant outcomes regarding the impact of BPSD on a person's autonomy. The main BPSD investigated in the studies were depression, apathy, irritability, agitation, aggression, disinhibition, and lability. Apathy had a recurrent association with reduced autonomy in persons with dementia, while depression and psychosis were also found to have an impact on individuals' autonomy.

Future Therapeutic Strategies for Alzheimer’s Disease: Focus on Behavioral and Psychological Symptoms

Alzheimer’s disease (AD) is a progressive, degenerative brain disorder that impairs memory and thinking skills, leading to significant economic and humanistic burdens. It is associated with various neuropsychiatric symptoms (NPS) such as anxiety, agitation, depression, aggression, apathy, and psychosis. NPSs are common in patients with AD, affecting up to 97% of individuals diagnosed with AD. The severity of NPS is linked to disease progression and cognitive decline. NPS in Alzheimer’s disease leads to increased morbidity, mortality, caregiver burden, earlier nursing home placement, and higher healthcare costs. Despite their significant impact, clinical research on NPS in AD is limited. In clinical settings, accurately distinguishing and diagnosing NPS related to AD remains a challenge. Additionally, conventional treatments for NPS in AD are often ineffective, highlighting the need for new therapies that target these specific symptoms. Understanding these comorbidities can aid in early diagnosis and better management of AD. In this review, we provide a summary of the various neurological and psychiatric symptoms (NPS) associated with AD and new candidates under development for the treatment of NPS based on their therapeutic targets and mechanisms. On top of the conventional NPS studied so far, this review adds recent advancements in the understanding of social functional impairment in AD. This review also provides information that can contribute to the advancement of studies and translational research in this field by emphasizing therapeutic targets and mechanisms of action focused on AD-related NPS rather than conventional mechanisms targeted in AD drug development. Above all, considering the relative lack of research in this new field despite the importance of clinical, medical, and translational research, it may increase interest in NPS in AD, its pathophysiological mechanisms, and potential therapeutic candidates such as molecules with antioxidant potential.

Frequency and Longitudinal Course of Behavioral and Neuropsychiatric Symptoms in Participants With Genetic Frontotemporal Dementia.

Behavioral and neuropsychiatric symptoms are frequent in patients with genetic frontotemporal dementia (FTD). We aimed to describe behavioral and neuropsychiatric phenotypes in genetic FTD, quantify their temporal association, and investigate their regional association with brain atrophy. We analyzed data of pathogenic variant carriers in the chromosome 9 open reading frame 72 (c9orf72), progranulin (GRN), or microtubule-associated protein tau (MAPT) gene from the Genetic Frontotemporal dementia Initiative cohort study that enrolls both symptomatic pathogenic variant carriers and first-degree relatives of known carriers. Principal component analysis was performed to identify behavioral and neuropsychiatric clusters that were compared with respect to frequency and severity between groups. Associations between neuropsychiatric clusters and MRI-assessed atrophy were determined using voxel-based morphometry. We applied linear mixed effects and generalized linear mixed effects models to assess the longitudinal course of symptoms. A total of 522 participants were included: 221 c9orf72 (138 presymptomatic), 213 GRN (157 presymptomatic), and 88 MAPT (62 presymptomatic) pathogenic variant carriers. Principal component analysis revealed 5 phenotypic clusters (67.6% of variance), labeled diverse behavioral, affective, psychotic, euphoric/hypersexual, and tactile hallucinations phenotype. In participants presenting behavioral or neuropsychiatric symptoms, affective symptoms were most frequent across groups (83.6%-88.1%), followed by diverse behavioral symptoms (68.4%-77.9%). In c9orf72 and GRN pathogenic variant carriers, psychotic symptoms (32.0% and 19.4%, respectively) were more frequent than euphoric/hypersexual symptoms (28.7% and 14.2%, respectively), which was the other way around in MAPT pathogenic variant carriers (28.6% and 23.8%). Although diverse behavioral symptoms were associated with gray and white matter frontotemporal atrophy, only a small atrophy cluster in the right thalamus was associated with psychotic symptoms. Euphoric/hypersexual symptoms were associated with atrophy in mesial temporal lobes, basal forebrain structures, and the striatum (p < 0.05). Estimated time to symptom onset, genetic group, education, and sex influenced behavioral and neuropsychiatric symptoms (p < 0.05). Particularly, in c9orf72 pathogenic variant carriers, psychotic symptoms may be starting decades before recognition of onset of illness. We identified multiple clusters of behavioral and neuropsychiatric symptoms in participants with genetic FTD that relate to distinct cerebral atrophy patterns. Their severity depends on time, affected gene, sex, and education. These clinical-genetic associations can guide diagnostic evaluations and the design of clinical trials for new disease-modifying and preventive treatments.

A comprehensive overview of neuropsychiatric symptoms in adolescents with 22q11.2 deletion syndrome.

The 22q11.2 deletion syndrome (22q11DS) is associated with a variety of neuropsychiatric outcomes that vary across deletion carriers. We adopted a dimensional approach to provide a comprehensive overview of neuropsychiatric symptom expression in adolescents with 22q11DS and further our understanding of the observed phenotypical heterogeneity. Participants were 208 adolescents with 22q11DS between 10 and 19years old. Semi-structured clinical interviews and IQ tests were used to quantify symptom expression on multiple symptom dimensions, some reflecting DSM-IV diagnostic domains. We investigated symptom expression in those with and without a formal DSM-IV classification and examined between and within symptom dimensions. We used correlation analyses to explore associations between different symptom dimensions. We demonstrated inter-individual differences in symptom expression, both between and within neuropsychiatric symptom dimensions. On most symptom dimensions, more than 50% of adolescents expressed at least one clinically relevant symptom. In addition, a significant proportion of youth without a formal DSM-IV diagnosis reported clinically relevant symptoms (e.g. >85% of those without an ADHD diagnosis reported ADHD symptoms). The exploratory correlation analysis indicated mostly positive correlations between symptom dimensions. The finding that most adolescents with 22q11DS express neuropsychiatric symptoms, even in the absence of a DSM-IV classification, has substantial ramifications for guiding adequate support. Findings may spur further research into the dimensional structure of neuropsychiatric symptoms in 22q11DS and aid in uncovering mechanisms that contribute to symptom expression. Ultimately, this provides leads to improve clinical care for 22q11DS and to understand phenotypical variation in other high-risk genetic variants.

Basal ganglia theta power indexes trait anxiety in people with Parkinson's disease.

Neuropsychiatric symptoms are common and disabling in Parkinson's disease (PD), with troublesome anxiety occurring in one-third of patients. Management of anxiety in PD is challenging, hampered by insufficient insight into underlying mechanisms, lack of objective anxiety measurements, and largely ineffective treatments. In this study, we assessed the intracranial neurophysiological correlates of anxiety in PD patients treated with deep brain stimulation (DBS) in the laboratory and at home. We hypothesized that low-frequency (theta-alpha) activity would be associated with anxiety. We recorded local field potentials (LFP) from the subthalamic nucleus (STN) or the globus pallidus pars interna (GPi) DBS implants in three PD cohorts: 1) patients with recordings (STN) performed in hospital at rest via perioperatively externalized leads, without active stimulation, both ON or OFF dopaminergic medication; 2) patients with recordings (STN or GPi) performed at home while resting, via a chronically implanted commercially available sensing-enabled neurostimulator (Medtronic PerceptTM device), ON dopaminergic medication, with stimulation both on or off; 3) patients with recordings performed at home while engaging in a behavioral task via STN and GPi leads and electrocorticography paddles over premotor cortex connected to an investigational sensing-enabled neurostimulator, ON dopaminergic medication, with stimulation both on or off. Trait anxiety was measured with validated clinical scales in all participants, and state anxiety was measured with momentary assessment scales at multiple time points in the two at-home cohorts. Power in theta (4-8 Hz) and alpha (8-12 Hz) ranges were extracted from the LFP recordings, and their relation with anxiety ratings was assessed using linear mixed-effects models. In total, 33 PD patients (59 hemispheres) were included. Across three independent cohorts, with stimulation off, basal ganglia theta power was positively related to trait anxiety (all p<0.05). Also in a naturalistic setting, with individuals at home at rest with stimulation and medication ON, basal ganglia theta power was positively related to trait anxiety (p<0.05). This relationship held regardless of the hemisphere and DBS target. There was no correlation between trait anxiety and premotor cortical theta-alpha power. There was no within-patient association between basal ganglia theta-alpha power and state anxiety. We showed that basal ganglia theta activity indexes trait anxiety in PD. Our data suggest that theta could be a possible physiomarker of neuropsychiatric symptoms and specifically of anxiety in PD, potentially suitable for guiding advanced DBS treatment tailored to the individual patient's needs, including non-motor symptoms.

Effect of a single-session mindfulness-based intervention for reducing stress in family caregivers of people with dementia: study protocol for a randomized controlled trial

BackgroundCaregiver stress can pose serious health and psychological concerns, highlighting the importance of timely interventions for family caregivers of people with dementia. Single-session mindfulness-based interventions could be a promising yet under-researched approach to enhancing their mental well-being within their unpredictable, time-constrained contexts. This trial will evaluate the effectiveness and feasibility of a blended mindfulness-based intervention consisting of a single session and app-based follow-up in reducing caregiver stress.Methods/DesignThe study is a single-blinded randomized controlled trial with two arms (intervention versus an education session on dementia care) and assessments at baseline, 8 weeks, and 6 months. The eligibility criteria include: family caregivers aged 18 years or older; providing care for an individual with a confirmed medical diagnosis of dementia for at least 3 months prior to recruitment, with a minimum of 4 hours of daily contact; and exhibiting a high level of caregiver stress. The intervention comprises a 90-minute group-based session with various mindfulness practices and psychoeducation. Participants will receive a self-practice toolkit to guide their practice over a duration of 8 weeks. Sharing activities will be implemented through an online social media platform. The primary outcome is perceived caregiving stress. The secondary outcomes include depressive symptoms, positive aspects of caregiving, dyadic relationship, trait mindfulness, and neuropsychiatric symptoms of care recipients. The feasibility outcomes include eligibility and enrollment, attendance, adherence to self-practice, and retention, assessed using mixed methods.DiscussionThe study will contribute to the evidence base by investigating whether a single-session mindfulness intervention is effective and feasible for reducing caregiver stress among family caregivers of people with dementia.Trial registrationClinicalTrials.gov, NCT06346223. Registered on April 3, 2024.

The Diagnostic Challenges of Late-onset Neuropsychiatric Symptoms and Early-onset Dementia: A Clinical and Neuropathological Case Study

The emergence of new-onset neuropsychiatric symptoms in middle age presents a diagnostic challenge, particularly when differentiating between a primary psychiatric disorder and an early neurodegenerative disease. The discrepancy between bedside clinical diagnosis and subsequent neuropathological findings in such cases further highlights the difficulty of accurately predicting pathology, especially when there are no evident focal lesions or changes in brain volume. Here we present the case of a 59-year-old woman with inconclusive neuroimaging who exhibited pronounced neuropsychiatric and behavioral symptoms initially suggestive of a mood disorder, then of behavioral variant frontotemporal dementia. However, upon autopsy, we identified coexisting Lewy body disease pathology and tau-related changes, including argyrophilic grain disease and primary age–related tauopathy. This case illustrates the challenges encountered when diagnosing late-onset neuropsychiatric symptoms, emphasizes the link between such symptoms and early-onset dementia and argyrophilic grain disease, and contributes to our understanding of the impact of mixed neuropathology in this population. Accurate diagnosis is essential for the development of molecular-specific therapies and, as well as for accurate prognosis and enrollment in clinical trials.

Characterizing the progression from mild cognitive impairment to dementia: a network analysis of longitudinal clinical visits

BackgroundWith the recent surge in the utilization of electronic health records for cognitive decline, the research community has turned its attention to conducting fine-grained analyses of dementia onset using advanced techniques. Previous works have mostly focused on machine learning-based prediction of dementia, lacking the analysis of dementia progression and its associations with risk factors over time. The black box nature of machine learning models has also raised concerns regarding their uncertainty and safety in decision making, particularly in sensitive domains like healthcare.ObjectiveWe aimed to characterize the progression of health conditions, such as chronic diseases and neuropsychiatric symptoms, of the participants in Mayo Clinic Study of Aging (MCSA) from initial mild cognitive impairment (MCI) diagnosis to dementia onset through network analysis.MethodsWe used the data from the MCSA, a prospective population-based cohort study of cognitive aging, and examined the changing association among variables (i.e., participants’ health conditions) from the first visit of MCI diagnosis to the visit of dementia onset using network analysis. The number of participants for this study are 97 with the number of visits ranging from 2 visits (30 months) to 7 visits (105 months). We identified the network communities among variables from three-fold collection of instances: (i) the first MCI diagnosis, (ii) progression to dementia, and (iii) dementia diagnosis. We determine the variables that play a significant role in the dementia onset, aiming to identify and prioritize specific variables that prominently contribute towards developing dementia. In addition, we explore the sex-specific impact of variables in relation to dementia, aiming to investigate potential differences in the influence of certain variables on dementia onset between males and females.ResultsWe found correlation among certain variables, such as neuropsychiatric symptoms and chronic conditions, throughout the progression from MCI to dementia. Our findings, based on patterns and changing variables within specific communities, reveal notable insights about the time-lapse before dementia sets in, and the significance of progression of correlated variables contributing towards dementia onset. We also observed more changes due to certain variables, such as cognitive and functional scores, in the network communities for the people who progressed to dementia compared to those who does not. Most changes for sex-specific analysis are observed in clinical dementia rating and functional activities questionnaire during MCI onset are followed by chronic diseases, and then by NPI-Q scores.ConclusionsNetwork analysis has shown promising potential to capture significant longitudinal changes in health conditions, spanning from the MCI diagnosis to dementia progression. It can serve as a valuable analytic approach for monitoring the health status of individuals in cognitive impairment assessment. Furthermore, our findings indicate a notable sex difference in the impact of specific health conditions on the progression of dementia.

Non-Pharmacological Exercise Randomized Controlled Trials in Alzheimer's Disease.

This narrative review aimed to summarize evidence on responses to exercise in pre-clinical Alzheimer's disease (AD) and on how long-term exercise programs work to improve neuropsychiatric symptoms and cognitive performance. We conducted a narrative review of the body of research on the benefits of long-term exercise programs in improving cognitive performance and reducing neuropsychiatric scores in patients with AD. Long-term exercise therapy appears to improve blood flow, increase hippocampal volume, and promote neurogenesis in patients with AD. Higher levels of physical activity are associated with a lower chance of developing the disease, and most prospective studies have shown that physical inactivity is one of the most prevalent modifiable risk factors for the development of AD. Exercise appears to be beneficial in improving cognitive function, a neuropsychiatric symptom of AD. Exercise has been shown to have fewer side effects, such as non-pharmacological effects and better adherence than medication. In this review, experts provided a snapshot and authoritative summary of evidence for non-pharmacological exercise in patients with AD based on the best synthesis efforts, identified the main knowledge gaps and relevant barriers, and provided directions for future research. Furthermore, experts in randomized trial designs provided practical details and recommendations for researchers working in this area, underscoring the importance of relevant topics.

Prevalent and persistent new-onset autoantibodies in mild to severe COVID-19

Autoantibodies have been shown to be implied in COVID-19 but the emerging autoantibody repertoire remains largely unexplored. We investigated the new-onset autoantibody repertoire in 525 healthcare workers and hospitalized COVID-19 patients at five time points over a 16-month period in 2020 and 2021 using proteome-wide and targeted protein and peptide arrays. Our results show that prevalent new-onset autoantibodies against a wide range of antigens emerged following SARS-CoV-2 infection in relation to pre-infectious baseline samples and remained elevated for at least 12 months. We found an increased prevalence of new-onset autoantibodies after severe COVID-19 and demonstrated associations between distinct new-onset autoantibodies and neuropsychiatric symptoms post-COVID-19. Using epitope mapping, we determined the main epitopes of selected new-onset autoantibodies, validated them in independent cohorts of neuro-COVID and pre-pandemic healthy controls, and identified sequence similarities suggestive of molecular mimicry between main epitopes and the conserved fusion peptide of the SARS-CoV-2 Spike glycoprotein. Our work describes the complexity and dynamics of the autoantibody repertoire emerging with COVID-19 and supports the need for continued analysis of the new-onset autoantibody repertoire to elucidate the mechanisms of the post-COVID-19 condition.

Acute and long-term SARS-CoV-2 infection and neurodegeneration processes—circulus vitiosus

The global pandemic of COVID-19 caused by SARS-CoV-2 has had a devastating impact. Although many survived the acute effects of the pandemic, a significant number of survivors, including those with only mild symptoms, are now experiencing a prolonged and debilitating post-viral syndrome known as LC/PASC (long COVID/post-acute sequelae of SARS-CoV-2). Typical symptoms of LC/PASC include fatigue, breathlessness, chest pain, impaired cognition, difficulty sleeping, fever and gastrointestinal symptoms. Anxiety and depression can also last for weeks to months and range from mild to disabling. The association between neuropsychiatric symptoms and SARS-CoV-2 infection raises questions about the possible routes of SARS-CoV-2 entry to the central nervous system (CNS) and long-term effects of the virus on the CNS, their molecular basis, and the potential risk of neuronal damage associated with the subsequent development of neurodegenerative diseases.

Neuropsychiatric symptoms following the consumption of Lanmaoa asiatica, a poisonous mushroom native to Yunnan

AbstractObjectivesTo describe and analyze the clinical characteristics and outcomes of Lanmaoa asiatica poisoning cases.MethodsWe conducted a retrospective study of Lanmaoa asiatica poisoning cases admitted to the emergency department of the First People's Hospital of Yunnan Province from January 2023 to December 2023.ResultsA total of 81 patients were admitted, with ages ranging from 14 to 84 years and a median age of 42.5 ± 14.6, predominantly female (72.8%). The peak poisoning cases were observed in July (n = 55, 67.9%). The commonest clinical presentation was the mixed neuropsychiatric and gastroenteritic type (64.2%), while 24.7% of patients presented with neuropsychiatric symptoms only and 11.1% of patients presented with pure gastroenteritic symptoms. The most common first symptom was visual hallucination (n = 56, 69.1%), followed by gastrointestinal symptoms such as nausea (n = 44, 54.3%) and vomiting (n = 36, 44.4%). Around 69.4% of patients had delayed onset of neuropsychiatric symptoms of 12–24 h after mushroom intake and 78.7% of patients had onset of gastroenteritic symptoms within 6 h after ingestion. Laboratory tests showed normal blood routine, liver function, kidney function, cardiac enzymes, and coagulation function. The median length of stay was 3 days, and no fatalities were reported.ConclusionsLanmaoa asiatica poisoning peaked in July. The commonest clinical presentation was the mixed neuropsychiatric and gastroenteritic type. The most common first symptom was visual hallucination. The incubation period for gastrointestinal symptoms was shorter than neuropsychiatric symptoms. Short hospitalization and absence of organ function damage was observed in Lanmaoa asiatica poisoning.

Exercise effects on neuropsychiatric symptoms and quality of life in mild cognitive impairment: a systematic review and meta-analysis.

Exercise is considered as a cost-efficient option for individuals with mild cognitive impairment (MCI). Although the potential benefits of exercise for improving cognitive function are recognized, its impact on neuropsychiatric symptoms (NPS) and the quality of life (QoL) in individuals with MCI remains unclear. This study aims to investigate the effects of exercise interventions on NPS, including depression, anxiety, sleep disorders, and the quality of life in individuals with MCI. There were 17 randomized controlled trials (RCTs) involving 1,575 participants were included. The findings indicate a small but significant positive effect of exercise on depression (standardized mean difference [SMD] = -0.47, 95% confidence interval [CI]: -0.73 to -0.21), but the quality of the evidence is low. Mind-body exercises were relatively more effective in alleviating depression. No significant improvements were observed in sleep disorders (SMD = -1.27, 95% CI: -2.80 to 0.26). Exercise improved anxiety in one study but had no effect in the other. It also improved quality of life in seven studies, with two showing no effect. The findings suggest that exercise, particularly mind-body exercises, can improve depression in individuals with MCI. However, the effect of exercise on anxiety, sleep disorders, and quality of life is still uncertain, necessitating additional research. These findings underscore the significance of integrating customized exercise programs in managing MCI to boost quality of life and mitigate NPS. https://www.crd.york.ac.uk/prospero/. ID: CRD42023445369.

Cognitive disorders in type 1 diabetes: Role of brain glucose variation, insulin activity and glucocorticoid exposure.

The number of patients with type 2 diabetes (T2D) and type 1 diabetes (T1D) is on the rise, partly due to a global increase in new T1D cases among children. Beyond the well-documented microvascular and macrovascular complications, there is now substantial evidence indicating that diabetes also impacts the brain, leading to neuropsychological impairments. The risk of developing neuropsychiatric symptoms is notably higher in childhood due to the ongoing maturation of the brain, which makes it more susceptible to damage. Despite this awareness, the specific effects of diabetes on cognitive function remain poorly understood. This review synthesizes literature on the impact of diabetes on cognition and its relationship with brain structural changes. It presents data and hypotheses to explain how T1D contributes to cognitive dysfunction, with a particular focus on children and adolescents. The emphasis on the pediatric population is intentional, as young diabetic patients typically have fewer comorbidities, reducing confounding factors and simplifying the investigation of cognitive alterations. We examine the roles of hypo- and hyperglycemia, as well as the emerging role of glucocorticoids in the development of neuropsychological disorders. When specific mechanisms related to T1D are available, they are highlighted; otherwise, data and hypotheses applicable to both T1D and T2D are discussed.