Estrogen fluctuations during menopause are linked to increased psychiatric symptoms like depression and anxiety. Depression rates in menopausal women are 2-3 times higher than in premenopausal women, primarily due to rapid estrogen changes. Estrogen affects emotional stability by regulating neurotransmitters, adjusting HPA axis sensitivity, and influencing neuroinflammatory and epigenetic pathways. Menopausal hormone therapy (MHT) is a key treatment, stabilizing neurotransmitter systems and HPA axis activity, but requires personalized and evidence-based approaches.

This paper aims to systematically summarize the association between estrogen fluctuations and menopausal psychiatric symptoms, elucidate the underlying physiological and molecular mechanisms driving these symptoms, and evaluate the therapeutic potential of MHT, so as to provide a robust theoretical basis for clinical decision-making in menopausal mental health management.

We performed a thorough review of peer-reviewed studies from medical and psychiatric databases, examining the connections between menopausal estrogen changes, neurotransmitter regulation, HPA axis function, neuroinflammation, epigenetic changes, and the effectiveness and safety of MHT for managing psychiatric symptoms. We prioritized high-quality clinical trials, epidemiological studies, and mechanistic research to ensure reliable evidence.

The review highlights that sudden estrogen changes during menopause disrupt serotonin and norepinephrine signaling, alter HPA axis activity, and trigger neuroinflammation and epigenetic changes, increasing the risk of depression and anxiety. Menopausal hormone therapy (MHT) can alleviate these symptoms by restoring neurotransmitter balance and normalizing HPA axis function. However, its effectiveness depends on factors like treatment timing, hormone type, and individual patient characteristics, including medical history and symptom severity.

Estrogen fluctuation is a significant modifiable risk factor for psychiatric symptoms during menopause, affecting neurotransmitter, endocrine, inflammatory, and epigenetic pathways. Menopausal hormone therapy (MHT) is effective for symptom management when personalized and administered within recommended timeframes. This underscores the importance of assessing estrogen levels and psychiatric symptoms in menopausal women to optimize MHT and enhance mental health outcomes.

Adolescence is characterized by heightened self-consciousness and sensitivity to social evaluations. During this period, hostile attribution bias-interpreting ambiguous social cues as hostile-can lower quality of life (QOL) and contribute to future mental health problems. Adolescents with autism spectrum disorder (ASD) show similar difficulties, often more pronounced due to their cognitive style and interpersonal vulnerabilities. Group cognitive behavioral therapy (CBT) aims to correct such biases through structured cognitive and social experiences. This study evaluated the psychological effects of group CBT on hostile attribution bias, social functioning, and QOL in adolescents and young adults with ASD traits.

We conducted an 8-session group CBT program focusing on hostile attribution bias and suspiciousness in 21 adolescents and young adults with ASD traits attending a hospital psychiatric outpatient department. The 15 participants who completed the program were included in analyzes. Psychological indices included hostile attribution bias (Ambiguous Intentions Hostility Questionnaire), social functioning (Social Responsiveness Scale, Second Edition [SRS-2]), and subjective QOL. Pre-post changes were quantified as change rates ((post - pre)/pre × 100). Group-level changes were tested with paired analyzes; exploratory associations among change rates were examined using Spearman correlations.

Group CBT significantly improved hostile attribution bias (effect size [ES] = 0.698, p = 0.017), social communication and interaction (SRS-2; ES = 0.780, p = 0.012), and subjective QOL (ES = 0.752, p = 0.011). Exploratory individual-level analyzes showed a discordant pattern: smaller reductions in hostile attribution bias (less negative change rates) were associated with greater increases in subjective QOL (ρ = 0.597, p = 0.019).

This pilot study suggests that group CBT may reduce hostile attribution bias and improve QOL and social functioning in adolescents and young adults with ASD traits. Notably, the positive correlation between hostile attribution bias change rates and QOL change rates suggests that greater QOL gains were not necessarily accompanied by larger reductions in hostile attribution bias, indicating that improvements in cognitive bias and perceived well-being may arise through partly distinct or non-linear pathways rather than a simple one-to-one relationship.

University Hospital Medical Information Network (UMIN000030140).

Elevated impulsivity and temporal processing deficits are key risk factors for adolescent non-suicidal self-injury (NSSI); however, their joint neural substrates and specific contributions to NSSI remain inadequately characterized. This study aimed to elucidate the behavioral and neural interplay between these cognitive domains in adolescents with NSSI.

We recruited 44 adolescents with NSSI and 37 typically developing (TD) controls. Participants completed the Barratt Impulsiveness Scale (BIS-11), a Choice Delay Task (CDT), and time perception assessments (discrimination and estimation tasks). A subsample (33 NSSI, 30 TD) subsequently underwent functional near-infrared spectroscopy (fNIRS) to monitor prefrontal hemodynamic responses during an oddball task, a paradigm assessing inhibitory control.

Compared to TD controls, adolescents with NSSI exhibited significantly elevated trait impulsivity (BIS-11), heightened delay aversion (preference for immediate rewards in CDT), impaired short-interval temporal discrimination (600ms), and a consistent underestimation of time intervals (7s, 12s, 34s, and 90s). Stepwise regression analysis identified BIS-11 scores, 600ms discrimination thresholds, and 90s estimation bias as significant predictors of NSSI. Neuroimaging revealed that the NSSI group showed lower accuracy on the oddball task and significant hypoactivation in the left dorsolateral prefrontal cortex (L-DLPFC). Crucially, reduced L-DLPFC activation was associated with greater time estimation errors (at 12s and 34s) and increased NSSI.

Adolescents with NSSI display a distinct neurocognitive phenotype characterized by high impulsivity and distorted time perception. These deficits may be associated with reduced activation in the L-DLPFC. Our findings suggest that NSSI involves a dual failure of inhibitory control and temporal processing, indicating that interventions targeting prefrontal regulation may offer novel strategies for risk reduction.

Gastrointestinal and psychological symptoms jointly motivate patients with irritable bowel syndrome (IBS) to seek medical care, with the latter often exacerbating the difficulty of achieving overall improvement. Although acupuncture has been shown to improve gastrointestinal symptoms in the general IBS population, the evidence in individuals with psychological disturbances remains insufficient.

This will be a placebo run-in, randomized controlled trial. After the 1-week sham acupuncture intervention run-in period, the 80 eligible IBS patients without strong placebo responses will be randomly assigned to the true acupuncture (TA) group and sham acupuncture (SA) group. During the 4-week intervention period, all patients will receive the assigned intervention three times per week, followed by an 8-week follow-up. The primary endpoint is the response rate, defined as the proportion of patients with a decrease of greater than or equal to 50 points in the IBS Symptom Severity Scale (IBS-SSS) score from baseline at week 4. Secondary outcomes include the response rates at other time points, original IBS-SSS scores, Hospital Anxiety and Depression Scale (HADS), Visual Analog Scale (VAS) for abdominal pain, satisfaction with bowel habits, blinding assessment, and Credibility/Expectancy Questionnaire. Safety will be monitored and recorded during the trial.

This trial will provide individualized evidence for addressing IBS with key comorbidities while excluding placebo response. The results of this trial will be published in a peer-reviewed journal.

https://itmctr.ccebtcm.org.cn/mgt/project/view/1985616257155727360, identifier ITMCTR2025002100.

Social media addiction (SMA) is often comorbid with anxiety and depression. This study examined the temporal stability of core SMA symptoms and the bridging symptoms with anxiety and depression.

A total of 1,240 adolescents (179 males, 1,061 females; mean age = 15.46 ± 0.63 years, age range: 14 - 18) completed the Bergen Social Media Addiction Scale (BSMAS), the Patient Health Questionnaire-9 (PHQ-9), and the Generalized Anxiety Disorder-7 (GAD-7) on two separate occasions in 2023 (T1) and 2024 (T2). The four symptom networks, including the BSMAS networks, two comorbidity networks (the BSMAS-GAD and the BSMAS-PHQ), and the integrated BSMAS-GAD-PHQ network, were estimated using Gaussian graphical models. Core symptom centrality was assessed using Expected Influence (EI), whereas bridge symptoms were identified using Bridge Expected Influence (BEI).

1) Although SMA, anxiety, and depression levels of respondents rose significantly over the year, all four networks showed strong temporal stability, with the edge weights (r = .892 -.973, p < .001), the EI (r = .806 - .961, p ≤ .002), and the BEI (r = .699 - .804, p ≤ .008) highly correlated between T1 and T2; network comparison tests showed no significant changes in overall structures of all four networks, with most edges showing stable weights. 2) Within the BSMAS network, BSMAS2 (tolerance) and BSMAS6 (conflict) exhibited the highest EI at both time points. 3) In the comorbidity networks, BSMAS3 (mood modification), BSMAS5 (withdrawal), and BSMAS6 (conflict) consistently served as bridge symptoms on the SMA side at both T1 and T2. 4) Across both time points, PHQ1 (anhedonia) and PHQ7 (concentration problems) exhibited the highest BEI on the depression side, whereas GAD1 (nervousness) and GAD5 (restlessness) did so on the anxiety side. 5) These bridge symptoms were also confirmed in the integrated network.

These findings illuminate the temporal persistence and development of symptom relationships, offering a more dynamic understanding of SMA-depression-anxiety comorbidity in adolescents.

The neurobiological mechanisms underlying Attention-Deficit/Hyperactivity Disorder (ADHD) remain incompletely understood. Existing research has identified abnormalities in alpha rhythm among individuals with ADHD; however, its association with core symptoms lacks consistency, suggesting that enhanced alpha activity may represent a state-dependent compensatory manifestation. The family environment, particularly caregiver stress, is recognized as an important external factor influencing the development of children with ADHD, yet its potential role as a mediator between clinical symptoms and neural brain activity has yet to be systematically explored.

The study included 59 children with ADHD. Correlations among attention deficit scores (ADS), hyperactivity/impulsivity scores (HIS), various dimensions of caregiver strain, and posterior alpha power were analyzed, with Bonferroni correction applied to control for multiple comparisons. Subsequently, hierarchical regression and mediation modeling were employed to examine the mediating effect of caregiver strain.

No direct correlation was found between ADS and alpha power. A triangular pattern among symptoms, stress, and brain activity emerged: ADS showed strong positive correlations with all dimensions of caregiver strain, and subjective internalized strain (SIS) remained significantly positively correlated with alpha power even after correction. The mediation model indicated a suppression pattern, wherein the statistical association between ADS and alpha power was consistent with a positive indirect pathway via SIS, alongside a masked direct association, resulting in a non-significant total effect.

The findings suggest a model in which SIS is a key statistical mediator in the relationship between ADHD symptoms and specific neural oscillatory patterns, and highlight the plasticity of brain function in response to the family emotional environment.

This narrative review critically examines the fundamental principles and clinical applications of Brain-Computer Interfaces (BCIs) in neuroscience and mental health. We searched PubMed, Scopus, and PEDro databases using pre-defined keywords, with inclusion restricted to clinical studies. The manuscript provides an evidence-based assessment of current indications, technological limitations, and emerging solutions, offering insights into both the opportunities and challenges for clinical integration. Clinical decision-making pathways are outlined to guide the adoption of BCI technologies in patient care. This article aims to increase awareness among clinicians and to equip them with the essential knowledge required as BCI systems advance toward mainstream clinical use.

Negative affect (NA), encompassing heightened states of sadness, anxiety, and guilt, is a key symptom across a spectrum of internalizing disorders. Recent advancements in digital phenotyping (DP) and machine learning (ML) may enable the automatic detection of short-term fluctuations in NA through digital phenotyping, a prerequisite for Just-In-Time Adaptive Interventions (JITAI). Evidence on the prediction of momentary NA with DP is sparse, but it indicates that personalized ML models are required to account for individual heterogeneities. This preregistered study is the first to analyze data from the PREACT-digital project, encompassing 242 outpatient subjects diagnosed with internalizing disorders. We examined whether passive sensor data (heart rate, steps, mobility, physical activity) could predict momentary NA, as assessed via ecologically momentary assessments (EMA). Personalized and population-based ML approaches were trained on 19,792 pairs of DP data and NA ratings. We found that personalized ML approaches substantially outperformed population-based models. The best model, however, only marginally exceeded the benchmark, predicting per-person mean NA. Our findings emphasize the need for personalized ML in DP studies. Future efforts could incorporate richer or more raw data streams or test sequential modelling approaches to help clarify whether DP and personalized ML could reliably inform just-in-time, data-driven support for individuals affected by internalizing disorders.

Steven Hyman, former director of the National Institute of Mental Health (2012), argued that neuroscience research in psychiatry frequently inherits the DSM's assumption that disorders are discrete entities, even though empirical boundaries between conditions are often porous. In response, Hyman and colleagues advanced the Research Domain Criteria (RDoC), which organizes psychopathology around core neurobiological domains that cut across diagnoses. In a conceptually similar direction, Blum (1995) introduced Reward Deficiency Syndrome (RDS) as a transdiagnostic construct intended to unify substance-related and behavioral addictions. To date, PubMed includes more than 1,650 reports referencing "reward deficiency" and 281 specifically referencing RDS. Recent genome-wide association and pharmacogenomic findings in very large cohorts (88.8 million subjects) are interpreted as supporting dopaminergic dysregulation as a key phenotype underlying RDS vulnerability. The Genetic Addiction Risk Severity (GARS^®) panel was developed to estimate liability for RDS and "preaddiction." Notably, many conditions listed in DSM-5 share overlapping genetic polymorphisms, with frequent convergence on pathways involved in dopaminergic neurotransmission. Building on this framework, we propose a biphasic prevention and treatment strategy for both substance (e.g., alcohol, nicotine) and non-substance (e.g., highly palatable food/glucose-related) addictive behaviors. In the acute setting, harm-reduction approaches may require targeted modulation of postsynaptic dopamine receptors (D1-D5) within the nucleus accumbens (NAc). Over longer time horizons, however, durable recovery may depend on restoring dopamine signaling-specifically, promoting dopamine activation and release within the NAc to support dopamine homeostasis. Failure to balance short-term and long-term dopaminergic interventions may contribute to affective instability, maladaptive behavior, and, in vulnerable individuals, suicidal ideation. Individuals with serotonergic/dopaminergic receptor deficits and/or high catechol-O-methyltransferase (COMT) activity may be more likely to self-medicate using substances or behaviors that transiently increase dopamine release. A growing body of evidence suggests that increasing D2 receptor expression in genetically vulnerable populations could reduce addictive risk. Although D2 agonists can downregulate receptors in vivo, in vitro work indicates that sustained stimulation may promote receptor proliferation, and gene-transfer studies producing DRD2 overexpression reduce alcohol and cocaine seeking in rodent models. Finally, naturalistic dopaminergic repletion strategies may represent a safer long-term approach to normalize dopaminergic function, support recovery, and improve quality of life across RDS-related behaviors. (WC 286).

Breast cancer during pregnancy (BCP) is clinically rare. Its occurrence during a unique physiological period introduces pregnancy-related complications that can seriously affect maternal health. Diagnostic and treatment criteria are lacking. Nowadays, breast cancer (BC) has surpassed lung cancer and become the most common malignant tumor in the world, posing a serious threat to women's physical and mental health. BCP is a rare malignant tumor with unique characteristics for diagnosis and treatment. Diagnosing cancer at this particular time in a woman's life is a challenge in clinical management because of the need to ensure psychological safety and pregnancy status. Lack of systematic diagnosis and treatment plans can affect patient outcomes. By reviewing the literature at home and abroad, we summarized the status of diagnosis and treatment of BCP as well as the controversial issues for clinical application, highlighting the evolutionary trajectory of management strategies in this field.