Obsessive–compulsive disorder (OCD) is a chronic neuropsychiatric illness characterized by intrusive thoughts (obsessions) and repetitive acts (compulsions). Hyperactivity within the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC), structures in the cortico-striato-thalamo-cortical (CSTC) loop that affect inhibitory control, has been implicated in its pathophysiology (Zhang et al. Front Psychiatry 2019; 10 522). Deep transcranial magnetic stimulation (dTMS) is a modern variation on non-invasive brain-stimulation (NIBS) that, unlike other NIBS approaches, targets deeper cortical structures to alleviate OCD symptomatology (Laskov & Klírová Neurosci Lett 2021; 755 135906). Its efficacy has been proven in several RCTs and meta-analyses (Trevizol et al. J ECT 2016; 32 262-266; Cruz et al. Psychiatry Res 2022; 317 114869; Carmi et al. Am J Psychiatry 2019; 176 931-938).

Two dTMS coils cleared by the US FDA for OCD are available – The BrainsWay H7 coil and the MagVenture Cool D-B80 Double-Cone coil. The Double-Cone coil, approved in 2020 for adjunctive treatment, is electromagnetically less potent in OCD-associated brain structures stimulation than H7 (Tzirini et al. PLoS One 2022; 17 e0263145). We compared the clinical performance of these two coils in a preliminary analysis of an ongoing randomised, sham (placebo)-controlled study designed to identify neurobiological predictors of dTMS response.

Twenty DSM-5-diagnosed OCD patients underwent six weeks of dTMS. Ten received the Double-Cone stimulation [active n = 8, sham n = 2] and ten the H7 stimulation [active n = 8, sham n = 2] (Figure 1). Treatment response was defined as ≥ 35% reduction on the Yale–Brown Obsessive Compulsive Scale (Y-BOCS).

The highest responder rate occurred with active H7 stimulation (4/8; 50%), followed by active Double-Cone stimulation (1/8; 12.5%); no sham-treated patient responded (Figure 2). χ² tests showed no significant differences between coils (χ² = 2.50, p = 0.114) or between active and sham stimulation (χ² = 2.78, p = 0.095). Mean reduction in Y-BOCS (indicates improvement) was greatest in H7-active (19.5%), followed by H7-sham (16.2%), Double-Cone-sham (12.2%), and Double-Cone-active (4.7%). Figure 3 shows boxplots of percentage Y-BOCS reduction by study group. Logistic regression identified shorter OCD duration as a significant predictor of response (B = −0.12, p = 0.048). Younger age also favoured response (p = 0.071). Although type of stimulation and coil both favoured the H7 coil, these effects did not reach significance (p = 0.086 and p = 0.059, respectively).Image 1:Image 2:Image 3:

Although the difference between the coils didn’t reach significance, owing to the small sample size, our data suggest that the H7 coil may be more effective than the Double-Cone coil for OCD, and that shorter illness duration is associated with a higher likelihood of response.

M. Jakubec: None Declared, O. Laskov: None Declared, N.-A. Böhmová: None Declared, N. Biačková: None Declared, A. Čechová: None Declared, T. Novák: None Declared, M. Klírová Grant / Research support from: Received honoraria in the form of travel reimbursement from Brainsway Inc. (Israel) and consulting fees from BTL Industries JSC (Czechia) and Deymed (Czechia).

Schizophrenia with predominantly negative symptoms is highly disabling and lacks effective treatments. This gap underscores the need for biomarkers to guide novel approaches. Brain-Derived Neurotrophic Factor (BDNF), essential for neuronal survival and synaptic plasticity, is consistently reduced in schizophrenia, especially in those with prominent negative symptoms. Although its role as causative or epiphenomenal remains debated, its involvement in neurodevelopment and synaptic regulation makes it a strong candidate biomarker. Neuromodulatory interventions like rTMS and tDCS enhance neuroplasticity with emerging evidence in schizophrenia. The combination of HD-tDCS priming with iTBS offers a promising strategy targeting DLPFC hypoactivity, leveraging metaplasticity to potentiate BDNF-mediated plasticity. Investigating serum BDNF may provide insights into the biological underpinnings of neuromodulation & possibility of developing biomarker-guided precision psychiatry for schizophrenia.

1. To measure and compare serum BDNF levels before and after HD-tDCS (active/sham) priming followed by iTBS.

2. To examine the correlation between serum BDNF levels and clinical symptom severity, including PANSS and SANS scores.

A prospective hospital based double-blinded randomized controlled study with a sample size of 40, where the participants were divided into Active or Sham HD-tDCS primed iTBS stimulation groups for a total of 20 sessions over two weeks. Serum BDNF was quantified at baseline and after 4 weeks using Sandwich ELISA kits. Symptom severity was assessed with PANSS and SANS. Data were analyzed using paired and independent t-tests, along with correlational analyses.

At baseline, serum BDNF did not differ significantly between active and sham groups. After 4 weeks, BDNF increased significantly in the active group, while a non-significant decline was observed in the sham group. Between-group comparison at 4 weeks favored the active group but did not reach statistical significance. Correlational analysis showed baseline serum BDNF negatively correlated with total PANSS scores. Post-treatment, higher serum BDNF levels correlated with lower PANSS total, PANSS negative subscale, and SANS domains including affective flattening and alogia. These findings suggest that increases in BDNF are linked to reductions in overall symptom severity.

HD-tDCS primed iTBS significantly increased serum BDNF levels in patients with negative symptoms of schizophrenia, with higher BDNF associated with reduced clinical severity. While between-group differences were not statistically significant, the results suggest that BDNF may serve as a biomarker of neuromodulation-induced neuroplasticity. Future studies with larger cohorts and longer follow-up are required to validate these findings and explore prognostic applications.

None Declared

Depression plays a significant role in Alzheimer’s-type dementia(AD) and affects approximately one in five patients1 (Asmer MS et al. J Clin Psychiatry. 2018 Jul 31;79). On the other hand, depression is a risk factor for the development of dementia. Despite years of research and the discovery of numerous pathophysiological factors in their mutual influence, there is still no sufficiently reliable therapeutic approach2 (Lyketsos CG et al. Alzheimers Dement.2011;7:5). As a non-invasive brain stimulation method, transcranial pulse stimulation (TPS) is a novel procedure based on shock-waves and whose effects on cognition in AD patients show promising results in current studies3(Günes AR et al. Eur.J.N.2024;1468-1331), furthermore beneficial influence on affective symptoms were reported4 (Sprick U et al. Brain Stimul.2025;439).

In our observational study, we investigated the effects and safetiness of TPS on depressive symptoms in 100 patients who met the criteria for AD.

Each of the 100 patients (mean age: 73,5 years; gender ratio: 5:7 (m:f)) received a total of 6 treatments within 14 days (each session with 6000 pulses, energy level 0.25 mJ/mm² and frequency 4 Hz). On the basis of individual MRI scans neuro-navigation was used to apply pulses bilaterally in the frontal (including the dorsolateral prefrontal cortex) and parietal lobe as well as the precuneus area (Image 1). Written consent and the approval of an ethics committee were obtained for all patients. Before, during and immediately after the TPS intervention, the antidepressant medication of all patients remained unchanged. To assess the intensity of depressive symptoms the Beck Depression Inventory II (BDI-II) was used before the first and after the last treatment session.

36 patients had a score above 5 points in BDI-II which represents the lower threshold with an average of 18,1 points within this group, which corresponds to a mild depression. The BDI-II total score in the pre-post comparison showed a reduction in the mean value from 18,1 to 5,9 points indicating a score almost below the lower threshold (Image 2). 26 patients reported temporary mild side effects such as fatigue or a local feeling of pressure in the treated areas. There were no serious adverse effects detected in any patient.Image 1:

To our knowledge, this trial is the largest study to systematically investigate the effects of TPS on depressive symptoms in AD patients so far. The positive impact on depressive symptoms may be based in part on stimulation of the dorsolateral prefrontal cortex, which is a well established target region in the treatment of major depressive disorder using transcranial magnetic stimulation. TPS seems to be a safe approach to treat depressive symptoms in patients with AD. Further studies with a larger study population are necessary to confirm the safety and effectiveness of this novel method.

None Declared

The effects of intermittent theta-burst stimulation (iTBS), a form of repetitive transcranial magnetic stimulation, on the hypothalamic-pituitary-thyroid (HPT) axis are not well understood. This axis is frequently dysregulated in treatment-resistant depression (TRD). We previously demonstrated that the difference in thyrotropin (TSH) response to protirelin (TRH) between 23 h and 8 h on the same day (the ∆∆TSH test) is a highly sensitive chronobiological marker.

To evaluate the impact of iTBS targeting the left dorsolateral prefrontal cortex (LDPFC) on chronobiological HPT activity in hospitalized TRD patients.

Twenty-three TRD inpatients with abnormal ∆∆TSH values (< 2.5 mU/L) and HAMD-17 scores ≥ 18 were compared to 23 matched healthy controls (HCs). Patients received 20 iTBS sessions (one per weekday over four weeks) while maintaining stable antidepressant treatment. The ∆∆TSH test and HAMD-17 scores were assessed pre- and post-treatment. Response was defined as a ≥ 50% reduction in HAMD-17.

Baseline ∆∆TSH values were significantly lower in TRDs than in HCs (p < 0.00001, by U test). After iTBS treatment, patients showed a decrease in HAMD-17 scores (p = 0.0001, by T test) and an increase in ∆∆TSH values (p = 0.001, by T test)—although still remaining lower than those of HCs (p = 0.03, by U test). At endpoint, HAMD-17 scores correlated negatively with ∆∆TSH values (rho = -0.74, p = 0.0004). Fourteen patients (61%) normalized their ∆∆TSH, of whom 11 (78%) were responders; all patients who did not normalize their post-treatment ∆∆TSH (n = 9) were non-responders (p = 0.0003, by Fisher’s Exact test).

While the underlying mechanisms remain to be clarified, this pilot study suggests that successful iTBS treatment may help restore normal chronobiological function of the HPT axis in TRD patients, and that such restoration is associated with clinical improvement.

None Declared

Electroconvulsive therapy (ECT) is employed as an effective and safe treatment modality for schizophrenia(Pompili M, et al. Schizophr Res 2013; 146 1–9). Oxidative stress has been implicated in the pathophysiology of schizophrenia(Bitanihirwe BK, Woo T-UW. Neurosci Biobehav Rev 2011; 35 878–93). Thiobarbituric Acid Reactive Substances (TBARS) are widely used as a marker of lipid peroxidation(Grignon S, Chianetta JM. Prog Neuropsychopharmacol Biol Psychiatry 2007; 31 365–9), yet the impact of ECT on TBARS levels remains unclear.

This study aims to compare TBARS levels in inpatients with schizophrenia who received ECT (n=18) versus those treated pharmacologically without ECT (n=20), and to examine their associations with clinical parameters.

38 inpatients diagnosed with schizophrenia were included. 18 patients received ECT in addition to pharmacotherapy, while 20 received pharmacotherapy only. Blood samples were collected on the first and last days of hospitalization to measure serum TBARS. Sociodemographic and clinical data were recorded at admission and CGI (Clinical Global Impression), PANSS (Positive and Negative Symptom Scale) scales were applied. Analyses were conducted with SPSS v28. Non-normally distributed data (Shapiro–Wilk) were tested using Mann–Whitney U, Wilcoxon signed-rank, chi-square, Spearman correlation, and multiple linear regression; with significance at p<0.05. (The ethics committee approval number is TABED 1-24-306)

Of the 38 patients, 18 received ECT plus medication, while the remaining 20 received medication alone. No significant differences were found between groups in terms of age, total duration of disorder, years of education, PANSS, CGI scores, or suicide history (all p>0.05). However, clozapine use was higher in the ECT group (χ²=4.374, p=0.036). TBARS levels showed no significant change from admission to discharge in either group (ECT group: 756.5 vs. 768.5 nmol/L; Z=-1.136, p=0.256; pharmacotherapy group: 644.0 vs. 693.5 nmol/L; Z=-1.512, p=0.130). There was also a similar percentage change in TBARS levels between groups (%9.6 vs. %15.3; Z=-0.380, p=0.704). Negative correlations were found between TBARS levels and both age (ρ=-0.441, p<0.001) and the duration of the disorder (ρ=-0.333, p<0.05). Regression analysis showed suicide history as the only significant predictor of TBARS levels (β=-0.402, p=0.013).

TBARS levels did not significantly change following either ECT or pharmacological treatment in schizophrenia inpatients, suggesting limited impact of ECT on oxidative stress as measured by lipid peroxidation. However, associations with age, illness duration, and history of suicide suggest potential relevance of oxidative stress markers in subgroups of patients.

None Declared

Transcranial Magnetic Stimulation (TMS) is a safe, non-invasive neurostimulation technique increasingly used in psychiatry(Sierra P,et al. Psychiatric Q 2024;95:271–285).Despite the fact that clinicians’ decisions may be influenced by knowledge, practical challenges, expected outcomes, and cultural factors, these aspects are rarely investigated in neuromodulation research(Van der Groen O. Neuromodulation 2023;26:705–706). In addition to these factors, both patients and clinicians are increasingly turning to artificial intelligence to inform treatment decisions.

In light of the above,we aimed to assess both ChatGPT-4o’s attitude toward TMS and the knowledge and attitudes of psychiatrists in Türkiye regarding this treatment modality.

Psychiatrists working in Türkiye were recruited using convenience sampling, and the study was conducted via Google Forms.Participants rated their TMS knowledge on five items, yielding a composite score(score range:3–17). To evaluate attitudes toward TMS, the authors developed 10 items(score range:5–50). Attitude questions were administered to both ChatGPT and the participants.Descriptive statistics were computed for sample characteristics. Group differences were examined using the Mann–Whitney U test.Correlational analyses were conducted with Spearman’s correlation, and multiple linear regression analysis was employed to identify predictors of prejudice scores.(The ethics committee approval number is I04-302-25)Table 1.

Multiple linear regression predicting prejudice scores

A total of 130 psychiatrists participated (81 female,49 male). Of these, 50.8% were residents, 40.8% specialists, and 8.5% professors. Prejudice scores were negatively correlated with knowledge (ρ=–0.39, p<.001). Participants had a mean prejudice score of 17.33±5.88, while ChatGPT-4o had a score of 15. Participants with neuromodulation training had considerably lower prejudice scores (U=1106.5, Z=–4.342, p<.001), whereas knowledge scores did not differ significantly (p=0.32). Prejudice scores were lower in clinics with TMS access (50%) compared to those without (Prejudice:U=1212.5, Z=–4.203, p<.001). Multiple regression significantly predicted prejudice scores (F(4,125)=7.86, p<.001, R²=.20). Neurostimulation training and knowledge level were significant negative predictors (Table 1.).

Training in neuromodulation and clinical use of TMS appear to reduce prejudice toward this treatment. ChatGPT’s lower bias score suggests that AI could complement clinical decision-making processes.

None Declared

Bipolar disorder (BD) is a lifelong, recurrent condition with growing evidence supporting a neuroprogressive course, entailing the need to adopt staging models to guide stage-specific interventions1. Although different approaches have been proposed so far, their application remains limited and largerly based on clinical features. Recent advances in biological markers, neuroimaging, and artificial intelligence may enhance the precision of staging models, thus enabling more personalized treatment strategies2-3.

The study aims to: (1) longitudinally assess clinical stage progression in BD over an 18-month follow-up using the Kupka & Hillegers model; (2) investigate the contribution of epigenetic regulation, inflammatory markers, oral microbiota profiles, and structural and functional MRI connectomics to stage transitions; and (3) develop and validate supervised ML algorithms capable of integrating clinical, biological, and neuroimaging variables to provide individualized, data-driven predictions of stage progression.

The BOARDING-PASS is a multicenter, prospective, observational study aimed at advancing current knowledge of BD progression.The study enrolled 120 subjects (age 18-70 years), classified according to the Kupka & Hillegers’ staging model, and recruited from three secondary-level psychiatric services in Italy. The primary outcome is the longitudinal assessment of clinical stage progression over a 18-month period, with assessment conducted at baseline (T0), T1 (6 months), T2 (12 months), and T3 (18 months after baseline). At each time point, socio-demographic and clinical variables were collected, as well as clinical stages were assigned. Additionally, at T0, T2, and T3, structural and functional MRI scans and peripheral blood and unstimulated saliva samples were collected. Finally, all multimodal data were integrated within a supervised ML algorithm, with the goal of developing a refined, data-driven staging model for BD (Figure 1).

As of September 2025, all 125 participants have been enrolled, with >50% having completed 6-month follow-up and 25% reaching 12 months. Dropout rate remains <10%. Preliminary internal analyses on partial datasets suggest promising accuracy (>70%) in predicting stage transitions with supervised ML models.Image 1:

The BOARDING PASS project aligns with the growing need for a standardized, biologically informed staging framework that integrates clinical, inflammatory, epigenetic, and neuroimaging profiles. Incorporating these dimensions may significantly enhance the characterization of BD patients by identifying specific dysfunctional trajectories and overcoming the traditional, diagnosis-centered approaches, thus leading to more targeted and effective treatment strategies.

The study is funded by the European Union - Next Generation EU - NRRP M6C2 - Investment 2.1 - PNRR-MAD-2022-12376693.

N. Girone: None Declared, L. Cremaschi: None Declared, F. Martella: None Declared, B. Benatti Speakers bureau of: Angelini, Lundbeck, Janssen, Rovi, M. Cocchi: None Declared, A. Caporali: None Declared, S. Saluzzi: None Declared, C. Cavallotto: None Declared, I. Rosa: None Declared, A. Di Giorgio: None Declared, C. D’Addario: None Declared, M. Pettorruso Grant / Research support from: Angelini, Janssen-Cilag, and Lundbeck, Speakers bureau of: Angelini, Janssen-Cilag, and Lundbeck, F. de Pasquale: None Declared, G. Martinotti Grant / Research support from: Angelini, Doc Generici, Janssen-Cilag, Lundbeck, Otsuka, Pfizer, Servier, Recordati, Rovi, Viatris, Speakers bureau of: Angelini, Doc Generici, Janssen-Cilag, Lundbeck, Otsuka, Pfizer, Servier, Recordati, Rovi, Viatris, B. Dell’Osso Grant / Research support from: Rovi, Angelini, and Lundbeck, Speakers bureau of: Angelini, Janssen, Otzuka, and Lundbeck, Viatris and Bromatech

Cognitive deficits represent a critical therapeutic challenge in neurodevelopmental and neuropsychiatric disorders. Epigenetic modulation and histaminergic neurotransmission are both recognized as promising targets for enhancing cognition. A-366 is a potent dual G9a inhibitor and histamine H3 receptor antagonist with potential pro-cognitive properties. This study evaluated the therapeutic effects of chronic A-366 treatment on learning, memory, and oxidative stress in BTBR T+tf/J mice.

This study aimed to evaluate the effects of chronic A-366 treatment on cognitive performance and oxidative stress in the BTBR T+tf/J mouse model.

Male BTBR T+tf/J mice received chronic intraperitoneal administration of A-366 (0.5–2 mg/kg) for 21 days. Cognitive behaviors were assessed using the Fear Conditioning Test (FCT), Novel Object Recognition Test (NORT), and Open Field Test (OFT). Following behavioral evaluation, hippocampal tissues were analyzed for oxidative stress markers, including superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels.

Chronic A-366 treatment significantly enhanced cognitive performance in BTBR mice, as demonstrated by improved contextual and cued memory in FCT, higher discrimination indices in NORT, and preserved exploratory activity in OFT. Biochemically, A-366 increased SOD activity and decreased MDA levels in hippocampal tissue, indicating attenuation of oxidative stress.

A-366 exerts robust pro-cognitive effects in BTBR mice, potentially through dual modulation of epigenetic pathways and histaminergic neurotransmission, accompanied by restoration of oxidative balance. These findings highlight A-366 as a promising lead compound for the development of novel therapeutics targeting cognitive dysfunction in neurodevelopmental and neuropsychiatric disorders.

None Declared

Post-stroke depression (PSD), anxiety (PSA) and apathy are common and associated with poorer functional recovery and higher mortality. Recent evidence clarifies first-year trajectories and treatment effects, yet estimates vary across instruments and settings.

(1) Quantify 3/6/12-month prevalence and course of PSD, PSA and apathy; (2) identify independent 12-month predictors; (3) estimate absolute effects and safety of pharmacological and psychological interventions.

Databases: MEDLINE/PubMed, Embase, PsycINFO, Web of Science (2020–2025). Eligibility: adults with ischaemic/haemorrhagic stroke; longitudinal cohorts/registries, meta-analyses/IPD/meta-reviews, RCTs; validated 3–12-month outcomes. Exclusions: paediatric, case reports, non-validated tools, mixed neurological cohorts without stroke-specific data. Flow: 1,186 records; 864 after deduplication; 112 full texts; 17 included; 95 excluded. Populations: mean age 58–70 years; 38–50% women; inpatient/outpatient/community. Dual screening; narrative risk-of-bias (RoB2/ROBINS-I). Outcomes: prevalence/incidence, persistence/remission (pp), subgroup differences, absolute effects (ARR, NNT/NNH), adverse events.

PSD: pooled 27% (interview 24%, scales 29%); among ≤3-month cases, 53% persisted to 12 months and 44% remitted; new-onset 3–12 months 9%; 71% of annual episodes began ≤3 months.

PSA: 20–25% in year 1; at 3–6 months some cohorts 35%, higher in women (44.5% vs 28.5% in ischaemic stroke); ≈24% at 12 months.

Apathy: 33.0% (95% CI 27.6–38.4); longitudinal 7% persistent-high, 33% moderate, 50% low/none; self-reported apathy rose: AES 10.8%→22.4% (+11.6 pp); DAS 3.6%→11.0% (+7.4 pp) by 12 months.

Predictors (12 months): higher baseline NIHSS/mRS, cognitive impairment, prior affective disorder, low social support; sex differences mainly ischaemic (not consistent in haemorrhagic).

Interventions: fluoxetine 20 mg for 6 months vs placebo reduced new depression at 6 months 13.42%→10.05% (ARR 3.37%; NNT=30) with no functional benefit, but increased adverse events—fractures 1.39%→3.15% (NNH=57), injurious falls 4.51%→6.26% (NNH=57), seizures 1.80%→2.64% (NNH=119), hyponatraemia 0.61%→1.22% (NNH=164). Psychological therapies (CBT/behavioural activation), national routine-care dataset (n=7,597): 71.3% reliable improvement, 49.2% reliable recovery (associative, non-randomised), better when initiated ≤6 months. Adherence/discontinuation not consistently reported.

Within 12 months post-stroke, PSD ≈27%, PSA 20–25% and apathy ≈33%. Depression starts early and persists in ~1/2 early cases; apathy is comparatively stable and less treatment-responsive. Stepwise screening at 0–3–6–12 months, stratification by neurological severity/cognition and proactive social-support enhancement are warranted. SSRIs: small preventive benefit with safety trade-offs; psychological therapies: meaningful gains—integrate early.

None Declared

Up to 10–30% of stroke survivors develop dementia. Loneliness has been shown to be a psychosocial risk factor for developing stroke and cognitive impairment in the general population. Stroke survivors are more likely to experience loneliness. However, the contribution of loneliness to post-stroke dementia risk remains unclear.

We aimed to investigate the association between loneliness and incident dementia in stroke survivors.

We included 7,267 UK Biobank (No. 93604) participants with prior stroke (mean age =60.5 ±6.9 years, 55.6% male) without baseline dementia. Loneliness was assessed via two self-report questions (frequency of feeling lonely and frequency of confiding in someone close) and defined as a score of 2 (lonely) vs <2 (not lonely). Incident post-stroke dementia (all-cause) was ascertained from hospital records and death registries. We used Cox cause-specific hazards models to estimate hazard ratios (HRs) adjusted for demographics, socioeconomic status, comorbidities, health behaviours and physiological covariates. We also performed a relative importance analysis to rank risk factors. We calculated the Percentage of Excess Risk Mediated (PERM) by grouping explanatory covariates into categories, such as medication, behaviors, and comorbidities.

Over a median 10.2-year follow-up, 290 stroke survivors developed dementia. Loneliness was significantly associated with a higher risk of dementia (fully-adjusted HR 1.67, 95% CI: 1.12–2.49). In a risk-factor ranking, loneliness was the second most important predictor of post-stroke dementia, ranking ahead of conventional factors such as hypertension and obesity. The association between loneliness and post-stroke dementia was magnified in stroke survivors (HR: 1.67, 95% CI: 1.12–2.49) compared to individuals without stroke (HR: 1.22, 95% CI: 1.07–1.39). 25% of the excess dementia risk associated with loneliness was attributable to diabetes-related factors, with the remainder largely explained by medication, behaviors, comorbidities, and other covariates.

Loneliness is an independent risk factor for developing dementia among stroke survivors. This association is partly mediated by modifiable behavioral and physiological pathways. Our findings highlight loneliness as a prominent, yet addressable, risk factor for post-stroke dementia, underscoring the importance of screening for feelings of loneliness in stroke aftercare.

None Declared

Anorexia nervosa (AN) is a severe psychiatric condition in which body image distortion is a particularly prominent symptom. Such distortions can reduce motivation to engage in treatment and hinder weight recovery. Importantly, the presence and intensity of body image distortion vary across individuals with AN, suggesting heterogeneity in the disorder’s neurobiological underpinnings. The salience network, which detects and prioritizes emotionally and physiologically relevant stimuli and processes internal body signals as well as external visual information, may contribute to body image distortions.

This study aimed to examine resting-state functional connectivity (rsFC) of the anterior cingulate cortex (ACC), a hub of the salience network involved in self-monitoring and cognitive control, in hospitalized female AN patients with (BD+) and without (BD−) pronounced body image distortion, to clarify its neurobiological mechanisms.

Twenty-six women diagnosed with restrictive-type AN underwent resting-state functional MRI scanning. Based on their scores from the Stunkard Figure Rating Scale, they were divided into two subgroups: BD+ (n=12) and BD− (n=14). Functional imaging data were preprocessed and analyzed using the CONN toolbox, employing a salience network connectivity analysis with the ACC as the seed region.

In cross-sectional analyses controlling for age, BD+ AN patients exhibited altered resting-state connectivity of the ACC compared to BD− AN patients. Specifically, BD+ patients showed significantly reduced rsFC between the ACC and the right superior and inferior lateral occipital cortex (sLOC, iLOC), as well as the bilateral superior/middle frontal gyrus (SFG/MFG). Conversely, they demonstrated significantly increased rsFC between the ACC and the right cerebellum (Crus I/II) (all p < 0.05, FDR-corrected).

The findings indicate that impaired top-down cognitive control over visual body perception and self-referential processing, coupled with over-engagement of cerebellar self-monitoring networks, may contribute to persistent body image distortions in AN. These findings align with the Allocentric Lock Hypothesis, suggesting that BD+ patients rely on internalized, memory-based representations rather than updating perceptions based on current visual feedback. The results highlight potential targets for personalized neuromodulation interventions in AN treatment.

None Declared

“Food noise” is an emerging term, originated from patient’s anecdotes, that inspired a wider conversation in the media and amongst clinicians. Since it is not a formal diagnosis, its definition varies throughout the available literature, one of them being “persistent thoughts about food that are perceived by the individual as being unwanted and/or dysphoric and may cause harm to the individual, including social, mental or physical problems”. It has become more noticeable through its sudden absence, reportedly following treatment with glucagon-like peptide-1 receptor agonists (GLP1-RAs). Understanding its neurobiological and psychopathological underpinnings may provide valuable insights for psychiatry and metabolic medicine.

This review aimed to synthesize current evidence on food noise, focusing on its conceptual definition, possible physiological and psychopathological mechanisms, and implications for clinical practice in psychiatry.

Original scientific articles and other relevant scientific publications indexed in the databases - PubMed, Google Scholar, ScienceDirect, and APA PsycNet – were analyzed. Preference was given to studies published in the last 10 years, written in English. Articles were examined for conceptual frameworks, neurobiological findings, and clinical implications related to food noise.

Food noise has been conceptualized as heightened reactivity to food cues, reflecting persistent activation of reward-related brain circuits (insula, amygdala, parietal cortex, hypothalamus). This state of reactivity can lead to food-related intrusive thoughts and negatively impact daily life, mirroring the preoccupation and disordered thinking observed in behavioral addictions and substance use disorders.

Functional MRI studies demonstrate that GLP-1 receptor agonists, such as liraglutide, modulate brain responses to highly palatable food cues, supporting a physiological basis for the reduction in food noise reported by patients. Preclinical and translational evidence suggests GLP-1 signaling influences dopaminergic and reward pathways, potentially attenuating compulsive behaviors beyond eating. Psychopathologically, food noise aligns with intrusive thought processes observed in eating disorders and obsessive-compulsive spectrum disorders.

Food noise is a psychological construct bridging psychiatry, neuroscience, and metabolic medicine. Although still colloquial, it may serve as a useful framework to understand intrusive food-related cognitions and their modulation by neurobiological pathways, particularly GLP-1 signaling. The role of food noise in weight management and mental health, as well as its social and cultural implications requires further research in order to validate operational definitions, develop standardized measures, and explore implications for diagnosis and treatment within psychiatric populations.

None Declared

Tardive dyskinesia (TD) is a persistent movement disorder associated with long-term antipsychotic (AP) use, often leading to physical, psychological, and social burden. In Europe, psychiatrists and movement disorder specialist neurologists (MDS neurologists) manage TD, but no formal treatment guidelines exist. Understanding specialty-specific differences in recognition and treatment is therefore important.

To understand standard-of-care approaches to TD between MDS neurologists and psychiatrists.

Psychiatrists and MDS neurologists in Italy, Spain, France, and the UK with experience managing TD completed a 25‐minute web‐based survey. Results were analyzed descriptively.

334 physicians (241 psychiatrists, 93 MDS neurologists) completed the survey. MDS neurologists reported a higher proportion of patients with TD in their clinical practice than psychiatrists. To diagnose TD, similar proportions of psychiatrists (52%) and MDS neurologists (47%) reported frequently using DSM-5 criteria. Both specialties estimated that most patients had mild or moderate TD, though MDS neurologists reported a larger proportion of severe TD (21% vs 15%). TD severity was commonly reported as influencing TD management strategy (psychiatrists: 82%; MDS neurologists: 70%), followed by the impact of TD on quality of life (76% vs 65%). For severe TD, psychiatrists were more likely to modify, switch or discontinue APs (55% vs 50%), while MDS neurologists more often prescribed add-on treatments (44% vs 37%). Both specialties reported similar patterns for utilizing the “watch and wait” approach (mild TD: 29–30%; moderate TD: 13%; severe TD: 7–8%). Across TD severities, anticholinergics and benzodiazepines were more frequently prescribed as an add-on treatment by psychiatrists, while tetrabenazine (TBZ) and amantadine were more frequently prescribed by MDS neurologists. Both groups rated TBZ and other off-label therapies only modestly effective, safe, and satisfactory (mean scores 4–8/10), underscoring the limitations of available options.

Psychiatrists more often modify AP treatment, while MDS neurologists favor pharmacological add-on therapies. Both prioritize TD severity in decision-making. These findings may help guide efforts to harmonize TD care across specialties and improve patient outcomes.

A. Fagiolini Grant / Research support from: Angelini, Boehringer Ingelheim, Idorsia, Italfarmaco, Lundbeck, Janssen, Medicamenta, Mylan, Otsuka, Pfizer, Recordati, Rovi, Sunovion, Teva, and Viatris, Consultant of: Angelini, Boehringer Ingelheim, Idorsia, Italfarmaco, Lundbeck, Janssen, Medicamenta, Mylan, Otsuka, Pfizer, Recordati, Rovi, Sunovion, Teva, and Viatris, M. Driessen Shareholder of: Teva Pharmaceuticals, Employee of: Teva Pharmaceuticals, A. Guevara Morel Shareholder of: Teva Pharmaceuticals, Employee of: Teva Pharmaceuticals, M. Konings Shareholder of: Teva Pharmaceuticals, Employee of: Teva Pharmaceuticals, K. Duma Shareholder of: Teva Pharmaceuticals, Employee of: Teva Pharmaceuticals, S. Reed Employee of: Oracle Life Sciences, P. Le Calvé Employee of: Oracle Life Sciences, A. Sadou Employee of: Oracle Life Sciences, S. Pappa Grant / Research support from: Johnson & Johnson, Lundbeck, Otsuka, Recordati, Rovi, Sunovion, and Teva Pharmaceuticals, Consultant of: Johnson & Johnson, Lundbeck, Otsuka, Recordati, Rovi, Sunovion, and Teva Pharmaceuticals

Oxytocin, a neuropeptide traditionally associated with social bonding and reproductive functions, has emerged as a critical modulator of anxiety and social cognition. Recent paradigm-shifting research has revealed that astrocytes, previously considered passive support cells, are essential mediators of oxytocin’s anxiolytic effects through novel signaling pathways distinct from neuronal mechanisms.

To synthesize current understanding of oxytocin receptor-mediated astrocytic signaling mechanisms, examine their role in anxiolysis, and evaluate therapeutic implications for social cognition disorders including autism spectrum disorder, schizophrenia, and ADHD.

Comprehensive literature review of peer-reviewed publications from major databases including PubMed, Nature, and specialized psychiatric journals. Analysis focused on molecular mechanisms of oxytocin receptor signaling, astrocytic pathways, anxiolytic mechanisms, and clinical applications in social cognition disorders.

Oxytocin receptor activation in astrocytes triggers a novel Sp1-Gem signalling cascade, distinct from neuronal pathways. This mechanism involves transcription factor Sp1 upregulation, increased Gem expression, and subsequent RhoA/ROCK pathway inhibition, leading to cytoskeletal remodelling and process elongation. Astrocytic oxytocin signalling modulates gap-junctional communication through connexin regulation and alters astrocyte-synapse spatial relationships. Astrocyte-specific knockdown of oxytocin receptors or Gem completely abolishes oxytocin’s anxiolytic effects, establishing astrocytes as necessary mediators. Clinical evidence demonstrates oxytocin’s therapeutic potential in autism spectrum disorder, with intranasal administration improving social cognition and reducing repetitive behaviors.

The discovery of astrocytic oxytocin signaling represents a fundamental paradigm shift in understanding anxiolytic mechanisms. The Sp1-Gem pathway offers novel therapeutic targets for anxiety and social cognition disorders, potentially enabling more precise interventions than global oxytocin administration. This research opens new avenues for treating neuropsychiatric conditions through astrocyte-specific modulation.

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Treatment-resistant depression (TRD) remains a major clinical challenge, with limited efficacy of available therapies. Psilocybin, a serotonergic psychedelic, has shown promising antidepressant effects. As recent studies have shown altered default mode network activity following psilocybin administration, further neuroimaging research in clinical populations is needed to clarify its mechanisms of action and the neural networks associated with symptom improvement in depression.

To investigate whether the antidepressant effects of psilocybin are associated with changes in resting-state brain activity and to assess the feasibility of conducting psilocybin trials in a French clinical population.

Patients meeting DSM-IV criteria for moderate to severe TRD underwent two fMRI sessions 2 days before and 5 days after a single oral psilocybin administration (25 mg). Amplitude of Low Frequency Fluctuations (ALFF) and regional homogeneity analyses were conducted to identify changes in resting brain activity after psilocybin.

Ten patients underwent the two fMRI sessions (8 women, 1 man; mean age 42.2 years). Resting-state analyses revealed increased ALFF signal in the right Ventro-Lateral Pre-Frontal Cortex (vlPFC) (Figure 1), the right Medial Pre-Frontal Cortex (mPFC) (Figure 2), and the left Inferior Parietal Lobule (IPL) (Figure 3) after psilocybin administration. Regional homogeneity analyses confirmed greater signal coherence in overlapping regions.Image 1:

Preliminary results from the PSILODAC study suggest that psilocybin modulates resting-state brain activity in patients with TRD. Upcoming analyses will include resting-state functional connectivity within positive valence circuits, as well as correlations between imagery outcomes and clinical response to psilocybin.

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Traditional smoking cessation methods—including pharmacotherapies and behavioral therapies—often fall short in achieving long-term abstinence. Pharmacologic interventions may not outperform placebo in real-world settings, and the safety and effectiveness of alternatives like e-cigarettes remain uncertain. Given the neurobiological underpinnings of nicotine addiction, repetitive transcranial magnetic stimulation (rTMS) has emerged as a promising noninvasive intervention targeting brain regions involved in craving, reward, and executive control.

To systematically evaluate the efficacy and safety of rTMS, including newer protocols such as intermittent theta burst stimulation (iTBS) and deep TMS (dTMS), for smoking cessation

We searched MEDLINE, Embase, PsycINFO, and CINAHL through March 2025 for English-language RCTs involving adult smokers treated with rTMS versus sham. Outcomes of interest included smoking abstinence rates, cigarette consumption, craving, and adverse events. Screening and data extraction were conducted by three independent reviewers using Rayyan, with conflicts resolved by consensus.

Seventeen studies involving 956 participants met inclusion criteria. Among them, 491 received active rTMS, and 448 received sham stimulation (data unavailable for 17 participants). The majority targeted the left dorsolateral prefrontal cortex (L-DLPFC), with protocols varying in frequency (1–20 Hz), intensity (80–120% rMT), and number of sessions (1 to 21). One study used iTBS, and two employed deep TMS targeting bilateral DLPFC and insula.

Cigarette consumption and craving significantly decreased in most active treatment arms compared to sham. Biochemically verified abstinence was significantly higher in select studies, particularly those using deep TMS. However, treatment effects often declined by 3- to 6-month follow-up. Across all trials, rTMS was well-tolerated, with no serious adverse events reported.

rTMS is a safe and potentially effective neuromodulatory intervention for reducing cigarette use, craving, and nicotine dependence. While short-term benefits are promising, long-term efficacy remains uncertain, and heterogeneity in protocols complicates direct comparisons. Deep TMS and theta burst protocols warrant further exploration in large-scale trials, particularly in diverse populations and those with comorbid psychiatric conditions.

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Research on visual evoked potentials (VEP) offers the possibility of finding electrophysiological markers of schizophrenia (SCH). VEP research has so far been limited to specialized laboratories. The development of a new portable device for the VEP measurement has brought the possibility of examining acutely ill patients. Previous research on VEP in SCH has shown a decrease in the amplitude of the P300 wave and a prolongation of the P300 latency as a promising endophenotype of SCH.

The aim was to measure VEP in hospitalized SCH patients and verify whether previously P300 connected findings also apply in this population. The mobile VEP device also allows for the determination of the speed of the motor response (i.e. reaction time, RT) to a visual stimulus. The secondary aim was to evaluate the relationship between physical parameters and immunological indicators (i.e. ratios of blood element counts from the blood count) with VEP values.

VEPs were measured in SCH patients hospitalized at the Dept. of Psychiatry of the Univ Hos in Hradec Králové. VEPs were also obtained from age and sex matched controls. The amplitude and latency of the P300 were evaluated. The motor response (button press) RT to a visual stimulus was measured. Other obtained values were: Body Mass Index (BMI), Positive and Negative Syndrome Scale (PANSS), Brief negative Symptom Scale (BNSS), Clinical Global Impressions-Severity (CGI-S) scales, B-CATS neuropsychological battery (containing tests TMT-A, TMT-B, Digit symbol, Animal naming), blood count.

Data from 60 patients and 60 healthy controls (HC) have been obtained so far. The P300 had a (p = 0.18) reduced amplitude, prolonged latency, and RT in SCH (both p < 0.001). RT increased faster (slowed down) in SCH in relation to age compared to HC. Moderate and weak correlations (Spearman’s rho) were achieved between cognitive test scores and VEP values. BMI was only weakly correlated with P300 amplitude, but not significantly correlated with other VEP values. Blood counts were also not significantly correlated with VEP values. BNSS and PANSS total scores both achieved moderate correlations with RT and with the difference in RT and latency. Olanzapine medication equivalent achieved only weak correlations with VEP. Correlations of VEP with CGI-S were only weak.Image 1:Image 2:

The faster RT slowing with increasing age in SCH compared to HC is a new finding. This may indicate faster brain aging in SCH. VEP values are apparently not distorted by BMI or blood count values. The achievement of moderate correlations with some cognitive tests, PANSS and BNSS values suggest the possibility of using VEP for quantifying both positive and negative and even symptoms of cognitive dysfunction in SCH. A deeper analysis of VEP recordings is needed to find more significantly correlating electrophysiological parameters compared to the currently used P300.

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Serum Sodium abnormalities are largely observed in older adults and are associated with higher risks. Less is known about the association between normal serum Sodium variations and medial temporal brain structures, mainly involved in cognition and memory.

The study’s objective was to explore the association between serum Sodium and Hippocampus volume and to assess associated cognitive risks.

Non-demented ADNI3 participants (healthy controls (HC) and those with mild cognitive impairment (MCI)) with complete serum Sodium, ADAS13 score, and Hippocampus volume at baseline were included. Linear and non-linear associations were evaluated. To assess the odds of MCI, logistic regression was performed.

A total of 469 cases with a median age of 70 years (IQR: 66, 76) were included. The median serum Sodium level was 141 (IQR: 139, 142). Serum Sodium levels showed a significant association with Hippocampus volume in the MCI subgroup (Adj.ßMCI=-95 (-162, -28), p=0.006, q=0.036).

Serum Sodium levels did not show a significant association with the ADAS13 total score (Adj.ßTotal=-0.04(-0.28, 0.21), p=0.8) or with the odds of being diagnosed with MCI at baseline (ORMCI= 1.00(0.88, 1.13), p= 0.935).

Normal serum sodium variations were significantly associated with hippocampus volumes, depending on the underlying neurodegenerative pathology, without predicting clinically relevant cognitive decline. Further studies are needed to better understand the mechanisms and identify protective factors.

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Functional Neurological Disorder (FND) is characterized by genuine neurological symptoms without structural explanation, often mimicking neuromuscular disease(Espay et al., 2018; Perez et al., 2021). Sarcoglycan Delta (SGCD) mutations cause limb-girdle muscular dystrophy type 2F (LGMD2F) in homozygous/compound heterozygous states, while heterozygotes are usually asymptomatic (Gordon et al., 2009). In contrast, Methylenetetrahydrofolate Reductase (MTHFR) polymorphisms are strongly associated with psychiatric vulnerability—including depression, schizophrenia, and bipolar disorder(Lewis et al., 2006; Meng et al., 2022)—suggesting predisposition for functional symptoms.

To highlight a case in which a 5-year history of gait disturbance was initially masked by incidental genetic findings, and to show how repeated examinations enabled FND diagnosis. The case underscores how functional symptoms affect electrophysiology, the need for psychiatric support, and challenges from genetic variants.

Comprehensive neurological, psychiatric, and genetic evaluations were performed.

A 48-year-old woman presented with a 5-year history of fluctuating gait disturbance, initially suspected as LGMD. Genetic testing revealed heterozygous SGCD and MTHFR variants. Neurological examination results varied: sometimes spastic and weak, sometimes (especially when distracted) completely normal. EMG performed during outpatient follow-up showed mild, non-specific proximal myopathic changes, whereas a repeat EMG during hospitalization was completely normal. Brain and spinal MRI were unremarkable, and antibody panels were negative. Following lumbar puncture, neurological symptoms spontaneously resolved. Psychiatric assessment revealed anxiety with preserved insight and judgment. Psychoeducation and psychotherapy were recommended.

This case demonstrates the diagnostic complexity when genetic findings suggest neuromuscular pathology but functional mechanisms predominate. SGCD heterozygosity represents a carrier state without overt disease, while MTHFR variants may increase psychiatric vulnerability and influence FND presentation (Gordon et al., 2009; Lewis et al., 2006; Meng et al., 2022). The patient’s 5-year fluctuating course, inconsistency between clinical examination and functional capacity, normal neuroimaging and electrophysiology, and transient improvement after lumbar puncture supported FND over neuromuscular disease (Espay et al., 2018; Perez et al., 2021). Recognizing positive diagnostic features—variability, reversibility, and internal inconsistency—is essential, as overinterpretation of genetic findings can lead to misdiagnosis, unnecessary interventions, and delayed psychiatric care. Multidisciplinary evaluation and timely psychiatric intervention are essential for accurate diagnosis.

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Telomeres, non-coding DNA sequences protecting the ends of chromosomes, are biomarkers of cellular ageing. Individuals with bipolar disorder (BD) have shorter telomere length (TL) compared to the general population, though the underlying molecular mechanism is unknown. TL homeostasis is regulated by 3 multiprotein complexes: the telomerase holoenzyme, the Shelterin and the CST complex. Lithium (Li) and valproic acid (VPA) are two commonly prescribed mood stabilizers for BD. Three studies has examined the potential protective effect of Li on TL or the expression of TERT (Telomerase reverse transcriptase), the catalytic subunit of telomerase in in-vitro models with conflicting results (Fries et al.j.jpsychires.2020),(Squassina et al. j.euroneuro.2016)(Squassina et al.Hum Genomics.2022). No data are available on other proteins within the three complexes, the measure of telomerase activity(TA) as well as on the effects of VPA.

This study aims to evaluate the impact of Li and VPA on the telomere homeostasis system in a neuronal in-vitro model.

SH-SY5Y neuroblastoma cells were cultured with Li or VPA at therapeutic range concentrations. Cells were collected after 7, 14 and 21 days of exposure. Then, measure of gene expression of 16 genes encoding proteins of the 3 complexes was conducted using RT-qPCR, measure of TERT protein levels using Wester-blot, telomerase activity (TA) analysis using a Telomeric Repeat Amplification Protocol assay and TL analysis using qPCR. Group comparisons were performed using the Kruskal–Wallis test with the R software.

No significant changes were identified between all analysed parameters of cells exposed to Li compared to controls at any time of exposure. However, for VPA, 7 out of 16 genes of the three complexess were altered at D7, D14 or D21 following distincts kinetics, including a downregulation of TERT (p=0.001). Additionally, at D21, TERT protein levels and TA were decreased compared to controls (p=0.02 and p=0.004). However, no changes in TL were observed at any time of exposure.

In the neuroblastoma model Li shows no protective effect on the telomere homeostasis system. VPA negatively impacts telomere homeostasis by limiting TA through the downregulation of TERT and a decrease in TERT protein levels at D21. It also alters the expression of multiple other genes within the three complexes. However, without significant changes in TL. The reduction in TA observed only at D21 suggests that a longer duration may be necessary to affect TL. The presence of alternative telomere lengthening mechanisms in SH-SY5Y cells (activated when TERT is supressed) could also explain these findings. Since the telomere homeostasis system is altered in cancer cells such as SH-SY5Y, similar analyses should be conducted in other in-vitro models with extended exposure durations.

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