Early detection of cognitive impairments is crucial for preventing progression to dementia. An effective diagnosis necessitates a tool with robust diagnostic characteristics. The Saint Louis University Mental Status (SLUMS) exam is a widely utilized instrument for diagnosing neurocognitive disorders. This study assessed the psychometric properties of its Persian version (P-SLUMS) among Iranian community.

This cross-sectional study was conducted with 450 community-dwelling older adults who were referred to one of the Tehran Municipality centers and participated in a cultural program from March to November 2021. Data collection tools included a demographic questionnaire, the Mini-Mental State Examination (MMSE) for concurrent validity, and the SLUMS exam. Dementia was assessed using the Persian version of the Global Deterioration Scale (GDS), while depression was evaluated with the Persian version of the Patient Health Questionnaire-9 (PHQ-9). The SLUMS exam was translated into Persian in accordance with the World Health Organization's protocol. Participants were recruited through convenience sampling based on the inclusion criteria. The P-SLUMS exam was evaluated for content validity, face validity, concurrent validity, and construct validity using Confirmatory Factor Analysis (CFA), as well as reliability, which was assessed over a two-week interval among 20 participants.

CFA indicated acceptable model fit indices. The goodness-of-fit indices for the model, including CFI, PCFI, and PNFI, were 0.82, 0.66, and 0.44, respectively, indicating a moderate fit that falls below the recommended thresholds for excellent parsimony. However, these indices are considered acceptable for our sample, which encompasses diverse education levels and a moderate number of items. The tool demonstrated high internal consistency (Cronbach's alpha = 0.866) and excellent test-retest reliability (ICC = 0.979).

The P-SLUMS exam is a valid, reliable, and user-friendly tool for early detection of Mild Cognitive Impairment (MCI) and dementia.

Fibromyalgia is a multifactorial syndrome characterized by chronic widespread pain, fatigue, and cognitive dysfunction that primarily affects women of working age. Because it lacks biological markers and its diagnosis is largely based on clinical criteria, fibromyalgia has been subject to gender biases that tend to minimize its symptoms and question the legitimacy of the condition. This delegitimization affects the employment trajectories of women with fibromyalgia, who experience higher rates of unemployment, withdrawal from employment, and discrimination. Studies indicate that only a minority are able to remain in the workforce and that many women feel compelled to conceal or minimize symptoms, which increases emotional exhaustion and worsens their health. In Chile, despite advances such as the enactment of Law 21,531 on fibromyalgia and non-cancer chronic pain, comprehensive programs integrating health and employment from a biopsychosocial perspective remain lacking. The aim of this article is to contribute to academic and social reflection on the occupational and psychosocial implications of fibromyalgia in women, highlighting the urgent need for inclusive strategies that support their ability to remain employed or return to work. Evidence indicates that employment plays a protective role by improving physical and mental well-being, providing economic independence, and fostering a sense of purpose. Therefore, the implementation of ergonomic interventions, reasonable accommodations, and psychoeducational strategies involving patients, families, health care teams, and employers should be prioritized. Only through inclusive policies with a gender perspective will it be possible to reduce occupational exclusion and improve the quality of life of individuals with fibromyalgia.

The aim of this study was to examine how a set of selected interacting maternal and perinatal clinical characteristics are associated with symptoms of post-traumatic stress after birth.

We conducted a cross-sectional online survey among women between 3 and 18 months after birth. Participants completed self-report measures of post-traumatic stress symptoms and questions regarding clinical variables related to pregnancy, birth and the postnatal period. Statistical models were used to estimate the association between clinical factors and symptom severity.

The strongest predictors of elevated post-traumatic stress symptoms were short-term complications like postpartum curettage and the need for hospitalisation due to neonatal health complications. Emergency caesarean section during the first stage of labour was also associated with higher symptom severity, whereas planned caesarean section, postpartum haemorrhage and prolonged postnatal stay were not significantly related to symptoms.

These findings highlight the importance of recognizing acute obstetric and neonatal events as relevant factors contributing to post-traumatic stress after birth. They specify that trauma-informed perinatal care must be actively implemented by establishing targeted psychological screening protocols for women experiencing emergency surgical interventions or neonatal separations, and by prioritizing transparent communication and continuous consent during acute obstetric procedures.

Substance-induced mental disorders (SIMD) are an under-recognized consequence of psychoactive substance use, despite major implications for treatment needs, health service demand and outcomes. In the context of British Columbia's (BC's) ongoing toxic drug emergency, we aimed to (1) estimate the incidence and prevalence of SIMD in the provincial population and (2) describe socio-demographic, geographic, clinical and substance-specific patterns over a two-year period.

We conducted a retrospective, population-based study using linked administrative health data from Population Data BC for residents aged ≥12 years between 1 January 2022 and 31 December 2023. SIMD cases were identified using a novel algorithm combining diagnostic codes with temporal linkage between substance-related events (poisoning, withdrawal or substance use disorder) and subsequent psychiatric diagnoses. Incident cases had no record of the same mental disorder in the previous two years; prevalent cases met SIMD criteria at any point in the study period. We calculated monthly, annual and cumulative incidence and prevalence rates per 10,000 population, stratified by sex, age group, health authority, urban/rural residence, neighbourhood income, psychiatric diagnosis, substance class, concurrent substance use disorder, involuntary treatment and mortality.

We identified 37,474 incident and 83,307 prevalent SIMD cases over two years, corresponding to a cumulative incidence of 77.5 and prevalence of 171.4 per 10,000 population. Monthly rates fluctuated in 2022, followed by a rise through 2023, with highest incidence (35.2 per 10,000) and prevalence (328.3 per 10,000) in May 2023. Males accounted for 62% of incident and 59% of prevalent cases; mean age was 43 years, with highest proportions in the 25-44 age range. Northern and Vancouver Island Health Authorities had the greatest burden. On average, individuals with SIMD had 3.2-3.6 healthcare visits per month. Cannabis- and hallucinogen-induced disorders were concentrated among younger people, while alcohol- and tobacco-related SIMD predominated in older adults; stimulant-related SIMD showed the highest hospitalization and involuntary treatment rates. Only about one-third of prevalent and fewer than one in five incident cases had a recorded concurrent substance use disorder.

SIMDs are common, clinically complex and unevenly distributed across demographic and geographic groups in BC. The high rates, substantial service use and frequent occurrence outside documented substance use disorder diagnoses underscore the need for improved detection of SIMD, integration of psychiatric and addiction care and regionally tailored prevention and treatment strategies within the ongoing toxic drug emergency.

Premenstrual dysphoric disorder (PMDD) is a condition linked to the menstrual cycle and characterised by cyclic emotional distress, irritability and anger, which can disrupt social functioning. Intermittent selective serotonin reuptake inhibitor treatment is effective in alleviating symptoms, yet the neural underpinnings of its efficacy in PMDD remain unknown.

This randomised, placebo-controlled trial aimed to evaluate the impact of intermittent escitalopram treatment on PMDD symptoms and aggressiveness, and on neural responses to social provocation.

Women with PMDD were randomised to receive either intermittent escitalopram (20 mg/day) or placebo during the luteal phase. Outcomes of interest were changes in mood (assessed by the Daily Record of Severity of Problems), self-rated state aggression (measured by the Aggression Questionnaire) and neural responses to aggression-related stimuli, captured by functional magnetic resonance imaging during the Point Subtraction Aggression Paradigm.

Intermittent escitalopram treatment significantly reduced PMDD symptoms compared with placebo, in particular irritability or anger (Cohen's d = -0.93, 95% CI [-1.48, -0.38]). Aggressiveness, which was positively associated with these symptoms (Pearson's r = 0.33, 95% CI [0.06, 0.55]), diminished following treatment (Cohen's d = -0.42, 95% CI [1.4 × 10^-4, 0.84]), with the reduction in irritability or anger partly mediating this association (standardised indirect effect -0.32, 95% CI [-0.77, -0.03]). Escitalopram treatment was nominally associated with lower reactivity to provocation in the anterior insula (involved in salience and threat detection) (Cohen's d = -0.34, 95% CI [-0.66, -0.02]), the activation of which was positively related to irritability or anger (Spearman's ρ = 0.39, 95% CI [0.07, 0.64]).

This randomised controlled trial provides timely confirmation of escitalopram as an effective treatment for PMDD within a contemporary clinical context and using prospective daily symptom ratings. Functional neuroimaging suggests that modulation of serotonergic function in PMDD is related to corticolimbic circuits involved in irritability or anger and interpersonal behaviour.

By studying changes in gene expression that occur without altering the DNA sequence, epigenetics offers a promising lead in unraveling how biological factors interact with the environment to shape brain development. However, prior developmental studies have focused on candidate brain or epigenetic regions, limiting our understanding of brain- and epigenome-wide links during childhood. This study explored associations between brain-wide structural imaging (T1-weighted, diffusion-weighted) and epigenome-wide DNA methylation in 144 children with and without ADHD, using parallel Independent Component Analysis (pICA) to identify linked patterns. We identified five significantly linked brain-epigenome components, in which methylation explains a significant proportion of variance in associated brain components, and further pinpointed 908 CpGs as part of the strongest epigenetic-brain associations using multivariate random forest analysis. Genes linked to these CpGs were enriched in neuronal development and associated with psychiatric/neurodevelopmental disorders, underscoring their functional relevance. Exploratory analyses suggested that ADHD diagnosis and demographic variables may modulate these brain-epigenome associations. Our study links brain anatomy to DNA methylation patterns in functionally relevant genes involved in neuronal development and psychiatric disorders, highlighting potential biological insights through which genetic and environmental factors may influence brain development. We further provide epigenetic to brain cluster mappings and a companion script to extract epigenetic-brain links, offering resources for future neurodevelopmental studies.

We aimed to investigate the associations between Alzheimer's disease (AD)-related blood biomarkers and changes in brain volumes and cerebrovascular burden in community-dwelling older adults.

We included 361 dementia-free participants with a Mini-Mental State Examination (MMSE) score ≥ 27 and without prior cerebrovascular events from a Swedish population-based study. Blood phosphorylated-tau217 (p-tau217), neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP) were measured at baseline. Brain magnetic resonance imaging (MRI) was performed at baseline and after 3 and/or 6 years. Linear mixed models were used to examine associations between AD-related blood biomarkers and changes in volumes of total brain tissue (TBTV), lateral ventricles, hippocampus, amygdala, and white matter hyperintensities (WMHs).

During the follow-up, higher p-tau217 was associated with faster volume loss in the hippocampus (β*year = -0.047, 95% confidence interval [CI] = -0.077 to -0.018) and in the amygdala (β*year = -0.064, 95% CI = -0.105 to -0.022). Elevated GFAP was linked to faster TBTV decline (β*year = -0.040, 95% CI = -0.059 to -0.021), ventricular enlargement (β*year = 0.028, 95% CI = 0.013 to 0.042), and hippocampal shrinkage (β*year = -0.038, 95% CI = -0.064 to -0.013). Participants with higher NfL showed steeper TBTV decline, ventricular enlargement, hippocampal and amygdala shrinkage, and faster WMH accumulation. Results remained largely consistent after excluding participants with mild cognitive impairment at baseline.

In cognitively unimpaired older adults, elevated blood p-tau217 was linked to faster shrinkage in AD-specific brain regions, whereas NfL and GFAP were associated with more widespread atrophy, with NfL also associated with accelerated WMH accumulation. These findings suggest that AD-related blood biomarkers may capture different dementia-related structural brain changes already at early stages. ANN NEUROL 2026.

Ubiquitination is a post-translational modification that governs various facets of eukaryotic biology, including protein stability, signaling, and immune regulation. The modification process is mediated by a coordinated enzymatic cascade, in which E3 ubiquitin ligases confer substrate specificity and determine the functional outcome of ubiquitin attachment. In the case of a virus infection, host cellular signaling networks undergo major ubiquitin-dependent changes to protect the host cell, including remodeling of cellular organelles, coordination of innate immunity, and reprogramming of metabolic pathways to prevent virus replication. African swine fever virus (ASFV) has evolved numerous strategies to counteract or evade these responses, thereby manipulating host defenses and promoting its replication. By modulating ubiquitination-dependent host cellular functions, the virus can regulate key immune signaling factors, suppress interferon production, and interfere with inflammatory pathways. These actions not only antagonize antiviral defenses but also remodel cellular homeostasis to favor infection. The important interplay between host defense and viral manipulation underscores the versatility of the ubiquitin system as a battleground in ASFV infection. In this review, we discussed mechanistic insights into how ASFV subverts ubiquitin pathways during host-virus interactions. This comprehensive knowledge might be beneficial for pharmaceutical exploration of host E3 ligase-dependent anti-ASFV treatment.

Background: Peptide receptor radionuclide therapy (PRRT) with ¹⁷⁷Lu-DOTATATE has become a cornerstone in the management of neuroendocrine tumors (NETs). However, the efficiency of this targeted therapy is highly dependent on the radiopharmaceutical drug delivery system and its infusion kinetics, which influence systemic biodistribution and therapeutic efficacy. This study evaluates various gravity-based infusion fluid dynamics to optimize the drug delivery profile, ensuring standardized delivery while minimizing residual activity. Methods: A retrospective analysis of 127 administrations of ¹⁷⁷Lu-DOTATATE (7.4 GBq per cycle) was conducted across 35 patients with NETs to assess vial dilution kinetics. Four distinct infusion rate (IR) strategies were compared to evaluate mass balance and delivery efficiency: constant infusion rate (1-IR); a single rate increase at 10 min (2-IR); two rate increases at 10 and 30 min (3-IR); and three rate increases at 10, 30, and 40 min (4-IR). Results: Stepwise increases in the IR significantly accelerated the vial clearance kinetics and reduced radiopharmaceutical stagnation within the infusion lines. Successful delivery of the target dose (98% of the pre-infusion activity measured in each specific vial) was achieved in 56% of cases with the 1-IR protocol (9 injections) and increased to 87% with 2-IR (45 injections), 97% with 3-IR (60 injections), and 100% with 4-IR (13 injections). Conclusions: Modulating fluid dynamics through stepwise IR protocols significantly enhances radiopharmaceutical delivery efficiency. The 3-IR protocol offers a favorable balance between procedural efficiency and clinical safety.

Sleep disturbances are highly prevalent across psychiatric disorders and represent both a clinical feature and a potential transdiagnostic therapeutic target. Growing evidence suggests that the gut microbiota may contribute to sleep regulation through immune, metabolic, circadian, and neuroendocrine pathways. Prebiotics, defined as selectively utilized substrates that confer health benefits through modulation of host microorganisms, have received increasing attention as nutritional strategies capable of influencing the gut-brain axis. This narrative review summarizes preclinical and human evidence on prebiotic interventions in relation to sleep-related outcomes and psychiatric symptomatology, with particular attention to short-chain fatty acids, circadian regulation, inflammatory pathways, stress-related hypothalamic-pituitary-adrenal axis activity, and microbial metabolite signaling. Preclinical studies suggest that selected prebiotics may influence sleep architecture, stress resilience, neuroinflammation, and behavioral phenotypes, particularly under conditions of stress or sleep disruption, but translation to human populations remains preliminary. Available clinical studies are limited by small sample sizes, heterogeneous prebiotic formulations, variable doses and intervention durations, inconsistent microbiome methodologies, and frequent reliance on subjective sleep measures rather than polysomnography or actigraphy. Therefore, current evidence supports prebiotics as biologically plausible and generally well-tolerated adjunctive strategies, but not as established treatments for insomnia or psychiatric symptoms. Sleep may provide a clinically meaningful transdiagnostic framework for future nutritional psychiatry research, provided that adequately powered randomized controlled trials integrate objective sleep assessment, standardized microbiome and metabolomic profiling, and clinically relevant psychiatric outcomes.