Longitudinal studies on population representative samples offer unique insights. The Estonian Children Personality Behaviour and Health Study (ECPBHS; EstChild) was launched in 1998 on two birth cohort samples at age 9 or 15 with an exceptional participation rate, has been monitored at ages 15, 18, 25 and 33, and also recruited parents of the target subjects. This multidisciplinary investigation has been focused on behavioural neuroscience, illuminating findings on what could be discerned from biomarkers, candidate genes, gene × environment interactions, and epigenetic markers in representative samples, and in birth cohorts living through societal transformation. ECPBHS analysed how biomarkers and lifestyle are associated with real-life behaviours and developmental trajectories, phenotypes such as neuroticism, bulimia, aggressiveness or attention deficit, and outcomes from incidence of psychiatric disorders to the obtaining of university education. Novel evidence has been observed on clustering of fears and the inner structure of impulsivity and reward sensitivity, together with clues how these may have co-emerged with metabolic types. New insights have been provided to understand the classic biomarkers, cholesterol and platelet monoamine oxidase activity, as well as several functional gene variants. Hypotheses how to synthetise molecular genetics and sociology, how sex or gender matters in the light of gene × environment interactions and how family and parental roles shape the behaviour of offspring have been put forward. The ECPBHS has offered clues on why in biological psychiatry many replication attempts are predestined to fail, and how to learn from such failures.

Investigating the relationship between behavioural 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 behavioural 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 is no recognised cure or specific biomarker for autism spectrum disorder (ASD). Exosomes are small vesicles that carry proteins, lipids and nucleic acids. They have been investigated for diseases such as Parkinson’s and Alzheimer’s. As the conclusions were on the biological utility of exosomes as a non-invasive brain biopsy, some animal, human and in vitro exosome studies have also been presented in the ASD field. The purpose of this review is to compile the studies that have established a relationship between ASD and exosomes so far and discuss their potential for linking the gap between the laboratory and clinic. In this systematic review, 31 PubMed articles were identified using the keywords ‘exosomal’, ‘exosome and ‘autism spectrum disorder’. After excluding 16 reviews, 4 irrelevant studies and 1 preprint, and adding 5 relevant articles, 15 research articles were included based on PRISMA criteria. The articles were investigated and reviewed by both authors. Their methodology and results are also discussed according to two main streams in studies. Numerous studies have identified potential biomarkers, including mitochondrial DNA (mtDNA7S), cytokines including IL-1β, TNF-α and IL-6, and different types of RNAs by comparing the exosomal contents of ASD patients or models with controls. In studies that focused on treatment, behavioural improvements were shown in ASD model mice. Since there are presently no reliable biomarkers or effective treatments for ASD, exosome-based research offers a promising avenue for early diagnosis and the creation of tailored therapies.

Autoimmune psychosis (AP) and other autoimmune psychiatric syndromes (APS) are associated with central nervous system antibodies. This study investigated related magnetic resonance spectroscopic imaging (MRSI) signatures and their correlations with electroencephalography (EEG), cerebrospinal fluid (CSF), and psychometric/neuropsychological measures. Twenty-eight adults with suspected antibody-positive AP spectrum syndromes were compared with 28 matched healthy controls. Inclusion in the patient group was based on the APS concept, resulting in a heterogeneous group with uniform autoimmunity. MRSI was performed using a spiral-encoded Mescher-Garwood localised adiabatic selective refocusing 3D-MRSI sequence. Glutamate+glutamine (Glx), gamma-aminobutyric acid (GABA), total N-acetylaspartate (tNAA), and total creatine (tCr) were reported as ratios to tNAA and/or tCr. EEG was analysed for intermittent rhythmic delta/theta activity (IRDA/IRTA) using independent component analysis. No significant differences in Glx, GABA, tNAA, or tCr ratios were observed between patients and controls. Correlation analyses in patients showed a trend for a negative association of the IRDA/IRTA rate before hyperventilation with the GABA/tCr ratio in both hippocampi and with the GABA/tNAA ratio in the left hippocampus and Glx/tCr ratio in the right putamen and pallidum. Significant positive correlations were observed between inflammatory CSF markers (white blood cell count and IgG Index) and GABA/tCr and GABA/tNAA ratios in the left caudate nucleus and right isthmus cingulate and thalamus, as well as between negative symptoms in PANSS and higher GABA/tCr ratios in the right putamen. No group differences were identified; however, correlations suggest a link between neuroinflammatory CSF markers and negative symptoms with GABAergic signalling in patients. Multimodal diagnostic approaches may provide a better understanding of the link between neuroinflammation, neurochemistry, and EEG slowing.

Extant literature implicates the role of glucagon-like peptide-1 (GLP-1) and GLP-1 receptor agonists (GLP-1RAs) on modulating alcohol-associated behaviours, with a particular emphasis of these agents on neural circuits subserving reward and appetite control. Herein, we explore the potential effects of GLP-1RAs on alcohol-associated behaviours in brain regions implicated in reward processing facilitating the repurposing of these agents for the treatment and prevention of problematic drinking. Understanding how GLP-1's analogues interact with alcohol-related behaviours may underscore the development of therapeutic strategies for alcohol use disorder (AUD) and those with comorbid metabolic disorders. A systematic review was conducted, wherein relevant literature was identified through Web of Science, PubMed, and OVID (MedLINE, Embase, AMED, PsycInfo, JBI EBP) from database inception to October 27th, 2024. Preclinical and clinical studies examining the association between GLP-1RAs and alcohol-related behaviours were assessed. Preclinical studies (n = 19) indicate that GLP-1RAs attenuate alcohol-related behaviours, with exenatide demonstrating significant dose-dependent effects in high alcohol-consuming phenotypes. Semaglutide and liraglutide are associated with reduced alcohol intake, though their effects were often transient. In human studies (n = 2) with AUD, semaglutide significantly reduced alcohol consumption, while exenatide showed mixed results, with reductions in alcohol drinking within high BMI subpopulations. Extant preclinical and clinical literature provides preliminary support for the potential therapeutic role of GLP-1RAs in attenuating alcohol consumption and preference. There is a need for large well controlled studies evaluating the effect of GLP-1RAs as a treatment strategy for behavioural modifications in individuals living with alcohol use disorder.

New developments in neuro-navigation and machine learning have allowed for personalised approaches to repetitive transcranial magnetic stimulation (rTMS) to treat various neuropsychiatric disorders. One specific approach, known as the cingulum framework, identifies individualised brain parcellations from resting state fMRI based on a machine-learning algorithm. Theta burst stimulation, a more rapid form of rTMS, is then delivered for 25 sessions, 5 per day, over 5 days consecutively or spaced out over 10 days. Preliminary studies have documented this approach for various neurological and psychiatric ailments. However, the safety and tolerability of this approach are unclear. We performed a retrospective study on 165 unique patients (202 target sets) treated with this personalised approach between January 2020 and December 2023. Common side effects included fatigue (102/202, 50%), local muscle twitching (89/202, 43%), headaches (49/202, 23%), and discomfort (31/202, 17%), all transient. The top 10 unique parcellations commonly found in the target sets included L8av (52%), LPGs (28%), LTe1m (21%), RTe1m (18%), LPFM (17%), Ls6-8 (13%), Rs6-8 (9%), L46 (7%), L1 (6%), and L6v (6%). Fatigue was most common in target sets that contained R6v (6/6, 100%) and L8c (5/5, 100%). Muscle twitches were most common in target sets that contained RTGv (5/5, 100%) and LTGv (4/4, 100%). These side effects were all transient and well-tolerated. No serious side effects were recorded. Results suggested that individualised, connectome-guided rTMS is safe and contain side-effect profiles similar to other TMS approaches reported in the literature.

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterised by impairments in social communication, repetitive behaviours, and restricted interests. Emerging evidence suggests that immune system dysregulation, particularly alterations in the complement system, may contribute to ASD pathophysiology. This study aimed to compare the serum levels of complement proteins (C1q, C2, C3, C4, MBL, L-ficolin, and hsCRP) between children with ASD and non-ASD controls. A total of 88 children (44 with ASD and 44 age- and sex-matched healthy controls) participated in this study. Complement protein levels were measured using enzyme-linked immunosorbent assay (from serum samples. The severity of ASD symptoms was assessed using standardised diagnostic tools, including the Childhood Autism Rating Scale, the Autism Behaviour Checklist, and the Repetitive Behaviour Scale-Revised. Serum C1q levels were significantly lower in the ASD group (p < 0.001). C3 levels were lower (p = 0.033), while C2 levels were slightly higher (p = 0.015) in the ASD group. There are no significant differences in C4, MBL, or L-ficolin levels. Logistic regression analysis identified reduced C1q levels as a significant predictor of ASD (p = 0.001). However, this study found no significant correlations between complement levels and ASD symptom severity scores. The findings suggest that alterations in complement system proteins, particularly reduced serum C1q levels, may be associated with ASD. Given C1q’s critical role in synaptic pruning and neuroimmune regulation, these results support the hypothesis that complement system dysfunction may contribute to the pathophysiology of ASD.

Acceptance and commitment therapy (ACT) is recognised as an effective treatment for a variety of mental illnesses. Several meta-analyses have reported the efficacy of ACT in various mental and physical conditions, including depression, anxiety, and pain, but not for suicidality. This study aimed to determine the therapeutic effectiveness of ACT on suicidality through a systematic review and meta-analysis. Electronic databases such as PubMed, Embase, Scopus, and the Cochrane Library were searched for studies. The primary outcome measure was the effectiveness of ACT for suicidality which includes suicidal ideations and attempts. This systematic review and meta-analysis included eight studies, all of which were judged to have a high risk of bias. In the meta-analysis, the pooled standardised mean difference for suicidal ideations was 1.122 (95% confidence interval (CI) = 0.261 to 1.982). This meta-analysis suggests that ACT is effective for reducing suicidal ideation, but the high risk of bias across studies should be considered as a major limitation. Further well-designed studies are needed to confirm these findings.

Suicidality is a significant public health concern, with neuroimaging studies revealing abnormalities in the brains of suicidal individuals and post-mortem samples. However, the genetic architecture between suicidality and subcortical brain volumes remains poorly characterized. Using genome-wide association studies (GWAS), we investigated the genetic overlap between suicidality and subcortical brain volume. GWAS summary statistics for suicidal behaviours, including Suicide Attempts, Ever Self-Harmed, and Thoughts of Life Not Worth Living, from the UK Biobank, Suicide from the FinnGen Biobank, and data on seven subcortical brain volumes and Intracranial Volume from the ENIGMA2 study, were used to investigate the genetic correlation between phenotypes as well as potential genetic factors. A common genetic factor was identified, comprising two categories: Suicide Attempt, Ever Self-Harmed, and Thoughts of Life Not Worth Living from the UK Biobank, and Suicide from FinnGen, Intracranial Volume, and subcortical brain volumes. Cross-phenotype GWAS meta-analysis of each category at variant, gene and subnetwork levels unveils a list of significant variants (P-value <5 × 10-8), and potential hub genes (P-value <0.05) of consideration. Network, pathway, and Gene Ontology analyses of these joint categories highlighted enriched pathways and biological processes related to blood-brain barrier permeability suggesting that the presence and severity of suicidality are associated with an inflammatory signature detectable in both blood and brain tissues. This study underscores the role of brain and peripheral blood inflammation in suicide risk and holds promise for developing targeted interventions and personalized treatment strategies to reduce suicidality in at-risk populations.

Selective serotonin reuptake inhibitors (SSRIs) have been associated with increased risk of osteoporosis, and sertraline may be more potent than citalopram in this regard. Here, target trial emulation was used to investigate whether sertraline, citalopram and escitalopram (the S-enantiomer of citalopram) differentially affect the risk of osteoporosis. Subsequently, it was examined whether SSRIs increase the risk of osteoporosis in a dose-response-like manner. Danish nationwide registers were used to identify all individuals that initiated treatment for depression with sertraline, citalopram, or escitalopram between January 1, 2007, and March 1, 2019. These individuals were followed until development of osteoporosis, death, or end of follow-up. Cox proportional hazards regression was used to adjust for relevant baseline covariates to emulate randomised treatment allocation to compare the rate of osteoporosis for individuals treated with sertraline, citalopram or escitalopram. Subsequently, the cumulative dose of sertraline, citalopram, and escitalopram was calculated, and Cox proportional hazards regression was used to assess dose-response-like relationships with osteoporosis. We identified 27,280, 65,529, and 17,703 individuals initiating treatment with sertraline, citalopram, and escitalopram, respectively. There was no material or statistically significant differential risk of osteoporosis between these groups (adjusted hazard rate ratio, aHRR = 0.98 for citalopram versus sertraline and aHRR = 0.94 for escitalopram versus sertraline). The results were not indicative of the SSRIs having a dose-response-like effect on osteoporosis risk. Sertraline, citalopram and escitalopram do not appear to differentially affect the risk of osteoporosis. The lack of clear dose-response-like relationships suggest that they do not have a causal effect on osteoporosis risk.