Acta Neuropsychiatrica最新文献

Background: Young adults (19-24 years) commonly experience elevated rates of sleep disturbance, anxiety, and cognitive stress yet often underutilise formal mental-health services. Music therapy, binaural beats, and related auditory entrainment techniques offer accessible, non-pharmacological approaches that may enhance emotional regulation, cognition, and physiological stability.

Objective: To systematically review interventional clinical trials published over the past decade evaluating music- and rhythm-based auditory interventions for mental-health and cognitive outcomes in young adults.

Methods: A systematic search of PubMed/MEDLINE and PsycINFO (01 January 2015 - 01 January 2025) was conducted using the terms (music therapy OR binaural beats OR auditory entrainment) AND (mental health OR neurorehabilitation OR cognition OR anxiety OR depression). After screening 122 abstracts, 10 trials met inclusion criteria. Effect sizes (Cohen's d) and 95% confidence intervals were extracted or estimated. Risk of bias was assessed using the Cochrane RoB-2 tool. The review protocol was registered in PROSPERO (CRD420251178490).

Results: Interventions included bedtime music therapy, audiovisual stimulation, and binaural-beat exposure across laboratory, clinical, and rehabilitation settings. Most studies demonstrated significant or moderate improvements in at least one domain: anxiety reduction, stress physiology, mood regulation, sleep quality or cognitive performance (standardised mean differences 0.3-0.6).

Conclusions: Evidence suggests that music-based and binaural-beat interventions can beneficially modulate sleep, anxiety, and cognitive processes in young adults. However, heterogeneity in design and small sample sizes limit the certainty of findings. Future adequately powered randomised controlled trials should address transdiagnostic mechanisms and long-term efficacy.

Background: This study investigated whether aspirin and atorvastatin provide additional antidepressant effects in patients with major affective disorders and inflammatory dysregulation.

Methods: Three 12-week treatment groups, each receiving aspirin (100 mg/day), atorvastatin (10 mg/day), or a placebo, were randomly assigned to 14 patients (seven with major depressive disorder [MDD] and seven with bipolar disorder [BD]), as well as two additional groups of 17 patients (each with nine patients with MDD and eight patients with BD). All patients had Clinical Global Impressions scores ≤3 and met the criteria for inflammatory dysregulation (i.e., C-reactive protein (CRP) level ≥ 1,000 ng/ml or soluble tumor necrosis factor-α receptor 1 (TNF-αR1) level ≥ 800 pg/ml). The Hamilton Depression Rating Scale (HDRS) and Montgomery-Sberg Depression Rating Scale (MADRS) were used to assess depressive symptoms, and the Global Assessment of Functioning Scale (GAF) was used to assess overall functioning. Baseline and week 12 CRP, TNF-αR1, and soluble IL-2 receptor (sIL-2R) levels were evaluated.

Results: Generalized estimating equation models demonstrated a reduction in total HDRS (p < 0.001) and MADRS (p < 0.001) scores and an increase in GAF scores (p < 0.001) in the medication groups compared with the placebo group. Only atorvastatin increased anti-inflammatory cytokine sIL-2R levels (p < 0.001). Both atorvastatin (p < 0.001) and aspirin (p = 0.025) raised proinflammatory cytokine sTNF-αR1 levels.

Discussion: Aspirin and atorvastatin improved depressive symptoms and overall function in patients with major affective disorders. However, both medications raised TNF-αR1 levels, and only atorvastatin increased sIL-2R levels.

Background: Schizophrenia (SCZ) shows marked biological heterogeneity, with negative symptoms linked to poor outcomes and hypothesized immune dysregulation. This study examined whether a peripheral cytokine-long non-coding RNA (lncRNA) panel could distinguish patients with SCZ and Brief Negative Symptom Scale (BNSS)-defined subgroups from healthy controls (HC).

Methods: Forty-one hospitalized patients with SCZ completed the BNSS and the Positive and Negative Syndrome Scale (PANSS). Twenty HCs, frequency-matched for age and sex, served as comparison samples. Severe negative-symptom subgroups were defined using two BNSS criteria: a broader (SNS1) and a more restrictive (SNS2) threshold. Serum cytokines-interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10)-and leukocyte lncRNAs (MALAT1, NEAT1, MEG3) were quantified by enzyme-linked immunosorbent assay and quantitative RT-PCR. Covariate-adjusted logistic and multinomial models (adjusting for age, sex, body mass index, and smoking) assessed discrimination using area under the receiver-operating-characteristic curve (AUC) and interquartile-range odds ratios (OR_IQR).

Results: IL-6 correlated with PANSS Total (ρ = .48, p = .001) and Negative (ρ = .34, p = .032) scores and was higher in SCZ than HC (p = .033), with further increases in SNS subgroups. NEAT1 was significantly reduced only within BNSS-defined subgroups (p ≤ .025). The dual-marker pattern (IL-6 ↑, NEAT1 ↓) showed the strongest discrimination for SNS1 versus HC (AUC = 0.85) and the steepest multinomial contrasts for SNS2 (IL-6 OR_IQR = 4.98; NEAT1 OR_IQR = 0.11).

Conclusions: Elevated IL-6 and decreased NEAT1 define a peripheral signature linked to negative-symptom severity in SCZ and may support biologically informed stratification and longitudinal research.

Background: Major depression (MDD) is linked to neuro-immune, metabolic, and oxidative stress (NIMETOX) pathways. The gut microbiome may contribute to these pathways via leaky gut and immune-metabolic processes.

Aims: To identify gut microbial alterations in MDD and to quantify functional pathways and enzyme gene families and integrate these with the clinical phenome and immune-metabolic biomarkers of MDD.

Methods: Shotgun metagenomics with taxonomic profiling was performed in MDD versus controls using MetaPhlAn v4.0.6, and functional profiling was conducted using HUMAnN v3.9, aligning microbial reads to species-specific pangenomes (Bowtie2 v2.5.4) followed by alignment to the UniRef90 v201901 protein database (DIAMOND v2.1.9).

Results: Gut microbiome diversity, both species richness and evenness, is quite similar between MDD and controls. The top enriched taxa in the multivariate discriminant profile of MDD reflect gut dysbiosis associated with leaky gut and NIMETOX mechanisms, i.e., Ruminococcus gnavus, Veillonella rogosaem and Anaerobutyricum hallii. The top four protective taxa enriched in controls indicate an anti-inflammatory ecosystem and microbiome resilience, i.e., Vescimonas coprocola, Coprococcus, Faecalibacterium prausnitzii, and Faecalibacterium parasitized. Pathway analysis indicates loss of barrier protection, antioxidants and short-chain fatty acids, and activation of NIMETOX pathways. The differential abundance of gene families suggests that there are metabolic distinctions between both groups, indicating aberrations in purine, sugar, and protein metabolism. The gene and pathway scores explain a larger part of the variance in suicidal ideation, recurrence of illness, neurocognitive impairments, immune functions, and atherogenicity.

Conclusion: The gut microbiome changes might contribute to activated peripheral NIMETOX pathways in MDD.

Objective: Investigating the relationship between behavioral addictions and mental health is essential due to their impact on well-being and the significant barriers they create to achieving lasting recovery. The aim of the study was to examine the prevalence of food addiction, problematic internet use, and internet gaming disorder among 866 high school students (grades 9-12) in Turkey, Bingöl and their associated with impulsivity, emotional regulation, depression, anxiety, and stress.

Methods: The sample was selected using a convenience sampling approach. Data were collected via online questionnaires using validated scales and analysed with SPSS package programme.

Results: The prevalence of food addiction was 6.9%, problematic internet use 14.3%, and internet gaming disorder 0.9%. Problematic internet use relatively high prevalence likely reflects adolescents' increased exposure to digital devices. Mental health factors were found to be significantly related to behavioral addictions: depression, anxiety, and stress predicted food addiction; depression and stress predicted problematic internet use, and anxiety was linked to internet gaming disorder.

Conclusions: This study contributes to the literature by examining multiple behavioural addictions and their common risk factors simultaneously and provides a comprehensive perspective. It is also one of the rare studies examining food addiction with other behavioural addictions. More research is needed to develop better intervention programmes and policies in the issue.

Objective: This study aimed to investigate the differences on cognitive performance across four cognitive domains – verbal memory, language fluency, visuospatial ability and cognitive inhibition – between drospirenone and ethinyl oestradiol (DRSP/EE) users and naturally cycling women in the luteal phase (LP). The goal was to determine whether hormonal suppression associated with DRSP/EE use is linked to domain-specific cognitive alterations.

Methods: A total of 48 young adult women were assessed: 23 using DRSP/EE (with pharmacologically suppressed endogenous hormonal levels) and 25 naturally cycling during the LP. Participants completed standardised neuropsychological tasks measuring verbal memory, language fluency, visuospatial ability and cognitive inhibition. Group comparisons analyses were conducted.

Results: Significant group differences were observed in verbal memory, visuospatial ability and cognitive inhibition, while no significant group differences were found in language fluency. Women using DRSP/EE showed significantly lower performance in verbal memory (U = 165, p = 0.009, r = 0.38) and visuospatial ability (U = 155, p = 0.006, r = 0.40) tasks compared to naturally cycling women. In contrast, they demonstrated higher performance in cognitive inhibition, quantified by a significantly higher Stroop interference score (t(46) = 2.710, p = 0.009, d = 0.783).

Conclusion: The present findings suggest that the use of DRSP/EE oral contraceptives is associated with differences across specific cognitive domains compared to naturally cycling women in the LP. The observed pattern – lower performance in hippocampus-related domains (verbal memory and visuospatial ability) paired with higher performance on a frontal-lobe-dependent task (cognitive inhibition) – is consistent with existing evidence suggesting that suppression of endogenous ovarian hormones may differentially influence cognitive functions. These behavioural associations underscore the need for further domain-specific research into the long-term cognitive implications of combined oral contraceptives.

Objective: Borderline personality disorder (BPD) is characterised by instability in interpersonal relationships, self-image, and affect. Dysregulated negative emotional processing involving prefrontal and limbic circuits is considered a neural basis of BPD. However, it remains unclear how prefrontal modulation of social decision-making in BPD differs from non-psychiatric controls.

Methods: To investigate social decision-making in response to unfairness, we conducted an functional magnetic resonance imaging study involving adults with a diagnosis of BPD (n = 77) and healthy controls (HCs; n = 60). Using an inequality aversion model, we derived parameters of social norm adaptation and inequality sensitivity from behavioural data during a modified ultimatum game designed to measure responses to offer norm shifts. Valence and salience signal-processing models isolated prefrontal activations related specifically to social norm prediction error.

Results: Cumulative rejection rates indicated that individuals diagnosed with BPD exhibited consistent differences in overall offer rejection rates but similar adaptation to HC when responding to norm shifts. Preservation of normative social decision-making in BPD (no significant difference vs. HC) was evident in regression analyses of rejection rates and in reinforcement learning models, with no group differences observed in Rescorla-Wagner parameters. Furthermore, we detected no significant neural activation differences between groups, although ventral regions of the medial prefrontal cortex were preferentially involved in valence-related rather than salience-related polynomial modulation.

Conclusion: Contrary to our hypotheses, neither behavioural nor neural responses to economic norm violations differed significantly between BPD and HC groups across one-shot games involving unknown partners. Future research could explore whether more personally relevant or higher-stress social contexts elicit differences not observed here.

Objective: Young-onset dementia (YOD), defined by symptom onset before age 65, encompasses diverse aetiologies and presents with prominent neuropsychiatric symptoms (NPS) that often accompany or exacerbate cognitive decline. However, the pathological mechanisms linking NPS, cognition, and biomarkers remain unclear. It was hypothesised that relationships between NPS and cognition would be mediated or moderated by cerebrospinal fluid (CSF) biomarker levels in individuals with YOD.

Methods: This retrospective, cross-sectional study included 46 participants with YOD (24 with Alzheimer's disease [AD], 22 with non-AD dementias) diagnosed at the Neuropsychiatry Centre, Royal Melbourne Hospital. NPS were measured using the Depression Anxiety and Stress Scale and Cambridge Behavioural Inventory-Revised. Cognition was assessed using standardised neuropsychological assessments. CSF amyloid-β (Aβ42), phosphorylated tau 181 (P-tau181), total tau (T-tau), and neurofilament light chain protein (NfL) were analysed. General linear models (GLMs) examined associations between biomarkers, cognition, and NPS.

Results: Higher P-tau181 (unstandardised beta [B] = -0.10, 95% confidence interval = [-0.20, -0.01]) and T-tau (B = -0.06 [-0.13, -0.01]) levels were associated with poorer memory recall in participants with YOD. In non-AD dementias, higher T-tau levels predicted greater NPS severity (B = 0.76 [0.06, 3.52]). NfL showed no significant associations with NPS or cognition.

Conclusion: Tau-related neurodegeneration (P-tau181 and T-tau) appears more closely linked to memory impairment in YOD than axonal injury markers such as NfL. In non-AD dementias, T-tau was additionally associated with behavioural symptom severity, suggesting tau-related mechanisms across subtypes. These associations require validation in larger, longitudinal, and multimodal studies to clarify temporal and mechanistic pathways.

The 22q11.2 deletion syndrome (22q11DS) is a genetic disorder characterised by defined microdeletions at chromosome 22q11.2. These genetic changes lead to a variety of neurodevelopmental problems, including cognitive delays and a very high rate of symptoms on the autism and schizophrenia spectrum. The underlying mechanisms contributing to these neurodevelopmental manifestations remain poorly understood. In concert with these neurodevelopmental difficulties there are also immune system alterations, including autoimmunity. We hypothesise that immune dysfunction and the presence of circulating autoantibodies may play a role in the pathophysiology of these neuropsychiatric symptoms. In this review, we synthesise the diverse literature on autoantibodies in 22q11DS and propose mechanisms for a causative role of these autoantibodies in neurobehavioural problems such as psychosis and cognitive delays. This review highlights the importance of further research to explore the interaction between autoreactive antibodies and functional alterations in neurocircuitry function. Understanding this relationship may provide insight into the origins of psychiatric symptoms.