Impaired autophagy has been implicated in the pathophysiology of neurodegenerative disorders, such as Alzheimer’s Disease (AD) and Parkinson’s Disease (PD). Consistent and replicated evidence indicate that Glucagon-like Peptide-1 Receptor Agonists (GLP-1RAs) exert treatment and preventative effects across disparate neurologic and mental disorders, potentially through mechanisms involving autophagy. This systematic review examined the effects of GLP-1RAs on autophagy in cell and animal models of AD and PD, as a proof of concept, to determine if these agents can be repurposed for the prevention and treatment of neurodegenerative and other mental disorders.

A systematic search on PubMed, Web of Science, and OVID (Medline, Embase, and APA PsycInfo databases) was conducted from inception to June 17, 2025. Screening was performed independently by two reviewers (MCS and IH) using predefined inclusion and exclusion criteria. Subsequently, a quality assessment was conducted.

The search yielded 142 studies, of which 14 were included. Across studies, GLP-1RAs (e.g., liraglutide, semaglutide, and exendin-4) autophagy-specific markers, including beclin-1, LC3-II/LC3-I, ATG7, ATG3, and LAMP1, while normalizing p62 levels.

In addition to promoting neurogenesis, neuroplasticity, and reducing inflammation, GLP-1RAs appear to modulate molecular and cellular systems contributing to autophagy, potentially mediating their broad therapeutic effects. Collectively, these studies present promising findings of GLP-1RAs for neurodegenerative and mental disorders; however, further studies are required to establish their translatability to human populations.

Electroconvulsive therapy (ECT) is an effective treatment of severe manifestations of mental illness. Since delay in initiation of ECT can have detrimental effects, prediction of the need for ECT could improve outcomes via more timely treatment initiation. Therefore, this study aimed to predict the need for ECT following admission to a psychiatric hospital.

This study was based on electronic health record (EHR) data from routine clinical practice. Adult patients admitted to a hospital within the Psychiatric Services of the Central Denmark Region between January 2013 and November 2021 were included in the study. The outcome was initiation of ECT >7 days (to not include patients admitted for planned ECT) and ≤67 days after admission. The data was randomly split into an 85% training set and a 15% test set. On the 7th day of the inpatient stay, machine learning models (extreme gradient boosting) were trained to predict initiation of ECT and subsequently tested on the test set.

The cohort consisted of 41,610 patients with 164,961 admissions. In the held out test set, the trained model predicted ECT initiation with an area under the receiver operating characteristic curve of 0.94, 47% sensitivity, 98% specificity, positive predictive value of 24% and negative predictive value of 99%. The top predictors were the highest suicide assessment score and mean Brøset violence checklist score in the preceding three months.

EHR data from routine clinical practice may be used to predict need for ECT. This may lead to more timely treatment initiation.

Self-regulation is central to adolescent emotional and cognitive development and deficits in self-regulation may associate with depression and anxiety. This scoping review maps the use of the Emotional Go/No-Go (EGNG), Delay Discounting Task (DDT), and Balloon Analogue Risk Task and Youth version (BART) in studies of adolescent depression and anxiety, examines consistency of task implementation, and identifies methodological and geographic gaps.

A PRISMA-ScR–compliant search was conducted in MEDLINE (PubMed), Scopus, and PsycINFO from database inception to 15 December 2025 (initial search: 1 December 2023; updated: 15 December 2025). Data were charted using a standardized form. Eligible studies included adolescents, employed EGNG, DDT, or BART, and assessed depressive or anxiety symptoms.

Thirty reports were included (EGNG n = 21; DDT n = 3; BART n = 6). Twenty-six studies (87%) were conducted in high-income countries and 24 (80%) were English language. Twenty-two studies were cross-sectional (EGNG n = 18/21; DDT n = 2/3; BART n = 2/6); five employed longitudinal designs, and two employed experimental manipulations. Fourteen studies (47%) reported significant task performance associations with depression or anxiety (EGNG n = 8/21; DDT n = 2/3; BART n = 4/6); remaining studies reported no significant associations. The directionality of associations differed across study populations and methodologies.

The current literature is concentrated in English-speaking higher-income contexts and has yielded few and inconsistent associations with adolescent depression and anxiety. Future research should harmonize protocols, expand evidence from low- and middle-income settings, and increase longitudinal and intervention-based studies to assess sensitivity to change and clinical utility.

This study aimed to investigate leptin (LEP) (G-2548A) and leptin receptor (LEPR) (668A>G) gene polymorphisms in SCZ patients with and without suicide attempts, compared to controls

The study included 120 patients with SCZ and 130 healthy volunteers. Sociodemographic characteristics, suicidal behavior, and symptom severity were assessed using data collection forms. Gene polymorphisms were analyzed from DNA samples using the polymerase chain reaction–restriction fragment length polymorphism.

The LEP genotype distribution in SCZ patients differed significantly from controls, with the heterozygous GA genotype more frequent in controls (p = .026). Within SCZ, LEPR genotype distribution differed by suicide attempt history; the heterozygous AG genotype was more frequent in non-attempters (p = .048). Logistic regression showed that the LEPR polymorphism (p = .023), number of hospitalizations (p = .036), and PANSS-psychopathology score (p = .023) predict suicide attempt history in SCZ.

Our findings suggest that LEP polymorphism may contribute to SCZ susceptibility, while LEPR polymorphism may be linked to suicide attempts in SCZ.

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.

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.

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).

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).

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.

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.

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.

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).

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.

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

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.

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

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.

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.

There are differences in IgA responses to tryptophan catabolites (TRYCATs) in major neurocognitive psychosis (MNP) versus simple neurocognitive psychosis (SNP) and normal controls. MNP and SNP are distinct schizophrenia classes which are differentiated by neurocognitive deficits, phenome features, and biomarker pathways. Nevertheless, there is no data on serum concentrations of those TRYCATs in MNP and SNP. The aim of the present study is to examine serum concentrations of tryptophan and TRYCATs in MNP versus SNP and controls.

This case-control study examines serum levels of tryptophan and TRYCATs in 52 MNP patients, 68 SNP patients and 60 controls in association with overall severity of schizophrenia (OSOS).

MNP patients show lower tryptophan, kynurenic acid (KA), 3-OH-anthranilic acid (3HAA), and higher anthranilic acid (AA) and quinolinic acid (QA) than SNP patients and controls. There were no differences between SNP and controls in these TRYCATs. Kynurenine (KYN) was lower in MNP+SNP than in controls. We found that 36.5% of the variance in OSOS was explained by the combined effects of lowered tryptophan, KA, and 3-HK, and increased QA and AA. The most important biomarkers of MNP and OSOS were the QA/KA ratio followed by the QA/3HAA ratio.

The alterations in serum TRYCAT levels further emphasize that MNP and SNP represent two biologically distinct subtypes of schizophrenia. The reductions in TRYCATs diminish the antioxidant and immunoregulatory functions of the TRYCAT pathway. Elevated QA levels may exacerbate the disruption of the blood-brain barrier and the immune-related and oxidative neurotoxicity in MNP.

Metabolic syndrome (MetS) is highly prevalent among adults and is frequently accompanied by depressive symptoms. While high-sensitivity C-reactive protein (hsCRP) has been proposed as a potential indicator of depression, existing evidence remains inconclusive.

This study aimed to determine whether increased serum hsCRP or other immune-metabolic biomarkers are associated with depressive symptoms in drug-naïve individuals with obesity and MetS.

A total of 88 drug-naïve patients with obesity and MetS but without coronary-artery disease were enrolled and serum levels of neuro-immune and metabolic biomarkers were assessed.

In MetS, the severity of depression, as assessed using the von Zerssen Depression Rating (VZDR) scale was significantly associated with interleukin (IL)-6, leukocyte numbers, triglyceride x glucose (Tyg) index, low-density lipoprotein cholesterol, Apolipoprotein B (all positively) and mean platelet volume (MPV), visfatin and adiponectin (all negatively). There were no significant associations between hsCRP and severity of depression. In MetS patients, hsCRP is strongly associated with increased leukocyte numbers, alkaline phosphatase, γ-glutamyl transferase, uric acid, platelet numbers and MPV, thereby shaping a distinct subtype of MetS, which is not related to depression.

Our findings indicate that depressive symptoms in MetS patients are associated with immune–metabolic biomarkers indicating immune activation, atherogenicity and insulin resistance, but not with hsCRP. The reason is that hsCRP in MetS is a biomarker of a specific MetS subtype that is characterized by megakaryopoiesis, hepatocyte activation, and uric acid production, which were not associated with depression.