The subtle, subjective nature of basic symptoms (BS) has often led to doubt regarding their clinical significance.

We therefore examined the prevalence, clinical significance and course of BS over three years in a large sample (N = 2684) of 16- to 40-year-old residents of the Swiss canton of Bern (response rate: 64%). At follow-up, persons with a lifetime risk symptom at baseline were compared with control subjects (N = 834; response rate 66%). Fourteen criteria-relevant BSs were assessed by trained clinical psychologists over the telephone, along with information on symptomatic ultra-high-risk symptoms, mental disorders and functioning.

At baseline, 18% of the participants reported any lifetime BS, 10% had still experienced one in the three months prior to the interview. In general, BS were rare, and only 2% of the participants met any BS criteria, which was significantly associated with non-psychotic mental disorders (OR = 5) and especially with functional deficits (OR = 16). At follow-up, five individuals had developed psychosis, one with BS criteria and three more with BS at baseline. In addition, 95% of the participants no longer met the BS criteria, while 3% reported new BS criteria.

Although BS are not rare phenomena in the community, they rarely persist and rarely occur frequently enough to meet the requirements of the risk criteria. Furthermore, they do not appear to occur randomly, but are restricted to a subpopulation of vulnerable individuals – possibly occurring in times of stress and/or low mood and functional difficulties in these individuals.

None Declared

Anxiety and depression are prevalent mental health conditions in patients with diabetes, significantly impacting their quality of life and complicating glycaemic control. The interplay between psychopharmacological agents and diabetes medications presents unique challenges in managing both mental health and metabolic conditions. This presentation reviews of psychotropic drugs commonly used to treat anxiety and depression in diabetic patients, with a focus on their efficacy, safety, and potential adverse effects. Special attention will be given to drug interactions between antidepressants, anxiolytics, and antidiabetic medications, which can influence treatment outcomes. Key considerations include the effects of psychotropic agents on insulin sensitivity, glucose metabolism, and the risk of hypoglycaemia. The presentation will also discuss personalized treatment strategies, adjusting for individual patient profiles and comorbidities. By integrating both psychiatric and endocrinological perspectives, we aim to improve clinical outcomes through optimized pharmacological management and minimize the risk of adverse drug interactions in this vulnerable patient population.

None Declared

Psychopharmacological treatment of anxiety and depression in patients with liver and/or kidney disease is complex, primarily due to the differences in pharmacokinetics compared to healthy individuals. Most medications are excreted via the kidney and/or liver, so dose adjustments are often necessary in these patients. Drug-drug interactions are also a significant clinical concern in liver and/or kidney disease, making regular monitoring essential. These factors may contribute to treatment relapse and severe adverse drug reactions associated with psychotropic medications and comedications.

Medication selection is, therefore, based on these considerations. Clinicians must regularly monitor kidney and liver function, although there are no clear global recommendations. A summary of product characteristics is the primary guideline for dose adjustments related to kidney and liver function, though it has limitations and is updated slowly. The most important monitoring parameters for these patients are liver enzymes and serum creatinine levels.

Patients with liver and/or kidney disease are often excluded from randomized controlled trials, meta-analyses, and clinical guidelines, resulting in a lack of data specific to this population. This issue is even more relevant in elderly patients treated with polypharmacy, as many somatic medications can worsen liver and/or kidney function in patients with anxiety and depression. In this context, some medications, such as vortioxetine, trazodone, agomelatine, quetiapine, and sertraline, are less affected by kidney disease in terms of pharmacokinetics.

Several tools are available for prudent medication selection and monitoring in these patients, including medication lists (e.g., Beers, Priscus), therapeutic drug monitoring (TDM), and collaboration with clinical pharmacists and/or pharmacologists. In this presentation, the presenter will discuss this topic from both pharmacological and clinical perspectives. Participants will learn the fundamental pharmacokinetic aspects necessary for medication selection in these patients, which are valuable for daily practice.

None Declared

Anxiety and depression are prevalent mental health conditions in patients with diabetes, significantly impacting their quality of life and complicating glycaemic control. The interplay between psychopharmacological agents and diabetes medications presents unique challenges in managing both mental health and metabolic conditions. This presentation reviews of psychotropic drugs commonly used to treat anxiety and depression in diabetic patients, with a focus on their efficacy, safety, and potential adverse effects. Special attention will be given to drug interactions between antidepressants, anxiolytics, and antidiabetic medications, which can influence treatment outcomes. Key considerations include the effects of psychotropic agents on insulin sensitivity, glucose metabolism, and the risk of hypoglycaemia. The presentation will also discuss personalized treatment strategies, adjusting for individual patient profiles and comorbidities. By integrating both psychiatric and endocrinological perspectives, we aim to improve clinical outcomes through optimized pharmacological management and minimize the risk of adverse drug interactions in this vulnerable patient population.

None Declared

Anxiety and depression are common psychiatric comorbidities in chronic medical illnesses, such as cardiovascular, endocrine, and neurological diseases. These conditions are associated with greater disease severity, poorer functional outcomes, and reduced quality of life for patients and their families. Despite their significant global burden, they are often underdiagnosed due to overlapping symptoms with primary medical conditions. Symptoms in medically ill patients may differ from classic psychiatric presentations, often involving heterogeneous (psycho)somatic phenomena like fatigue, autonomic irregularities, gastrointestinal symptoms, sleep disturbances, and cognitive impairments. Anxiety typically manifests as hypervigilance, excessive worry, and irritability, while depression presents with persistent sadness, psychomotor slowing, and loss of motivation, pleasure, and interest. Subsyndromal symptoms, though often untreated, can exacerbate functional decline and disease progression. Effective management requires a multimodal approach, with modern psychopharmacotherapy as a cornerstone. Selective Serotonin Reuptake Inhibitors (SSRIs) and Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) are recommended first-line treatments due to their safety and efficacy. In case of insufficient response, add-on strategies may include second-generation antipsychotics, lithium, esketamine, or pregabalin for predominant anxiety. Emerging evidence supports the use of phytotherapeutics as Silexan and Rhodiola rosea for subsyndromal symptoms. Non-pharmacological interventions also play an important role. Cognitive Behavioral Therapy remains the first-line psychotherapeutic option, complemented by mindfulness techniques, psychoeducation, biofeedback, and relaxation strategies, particularly for anxiety. Chronobiological treatments like bright-light therapy and sleep deprivation have proven effective for depression, especially in seasonal patterns. Brain stimulation methods, including transcranial magnetic stimulation and electroconvulsive therapy, may also be considered based on individual needs. Importantly, successful physician-patient interactions, directly and promptly addressing emotional and psychological concerns during consultations and daily rounds, are crucial in fostering treatment adherence and improving outcomes. In conclusion, anxiety and depression in medically ill patients present unique diagnostic and therapeutic challenges. Early recognition and individualized, multimodal treatment strategies can enhance adherence and outcomes. Integrating pharmacological and non-pharmacological approaches within collaborative care models and recommended treatment algorithms is essential for effectively addressing individual clinical presentations.

None Declared

The potential role of inflammatory and immune pathways in ADHD pathophysiology and pathogenesis has received considerable recent attention. Some of these pathways are long-studied in ADHD because of known or suspected mechanisms of high frequency comorbidities, such as obesity, sleep disorders, cardiovascular system disorders/migraine, atopic illnesses, and several autoimmune diseases. Aberrant cellular functioning, aberrant glial functioning, and/or aberrant mitochondrial dysfunction have all been implicated in mechanistic studies. While we separate these mechanisms conceptually, in reality they are intertwined and communicate with each other in a multi-directional complex of mechanisms.

To introduce the relationships among inflammation, immune mechanisms and ADHD, and provide a high level overview of current and cutting edge research in this area. We will review data linking ADHD with inflammation and immunologic mechanisms, recent findings on the genetic underpinnings of medical comorbidity in ADHD, and the relationship between maternal inflammation and genetic risk for ADHD in offspring.

This is a focused, narrative review of recent literature in the field.

Epidemiological, genetic, and biomarker data converge to illuminate the pleiotropic role of immune mechanisms in the pathophysiology of ADHD. Suspected mechanisms include both innate and adaptive pathways. Epigenetic vulnerabilities interact with environmental factors to confer greater risk for health problems among individuals with ADHD. Likewise, many of these same risk factors also carry increased risk for ADHD.

This information exemplifies the close relationship between psychiatric and medical conditions and/or their risk factors. The high heritability of the immune system and associated immunological dysfunctions provides a novel approach to understand the mechanisms through which gene-environment interactions may contribute to the occurrence and clinical presentation of ADHD.

None Declared

Attention-Deficit/Hyperactivity Disorder (ADHD) has been reported as a risk factor for COVID-19 infection and severity of illness. This presentation outlines the research trajectory that began during COVID-19 studies and has since demonstrated that ADHD is not only associated with an increased risk of infection but also with long-term COVID-19 syndrome (LCS). The chain of studies supporting these findings includes the association of ADHD with infections and inflammatory/autoimmune disorders, such as Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency and Familial Mediterranean Fever (FMF). These links, alongside globally reported associations between ADHD and other autoimmune disorders, such as Systemic Lupus Erythematosus (SLE), underscore the potential involvement of inflammatory and immune dysregulation in the pathophysiology of ADHD. The emerging data linking ADHD with inflammatory conditions—at both clinical and genetic levels—represents a significant new direction in ADHD research. Further investigation into these connections may provide deeper insights into the underlying mechanisms of ADHD and contribute to developing novel therapeutic strategies.

I. Manor Consultant of: Last three years: Teva Israel Ltd., Madison Israel Ltd., Takeda Israel Ltd., Peri Ltd., Mindtension Ltd.,

Clinical stageing models are well-established in many areas of medicine, most notably in oncology. These models are used to determine personalised treatment options and indicate prognosis. In psychiatry, staging models have been developed most prominently for psychosis and mood disorders. These models are being used to guide treatment and service provision, e.g. through development of high-risk and early intervention services and stage-appropriate treatment delivery. Clinical staging models for obesity, incorporating medical history, clinical and functional assessments and routine diagnostic investigations also exist and appear to show improved clinical utility in assessing obesity- related risk and prioritising treatment. Recent generic frameworks for staging in mental health have highlighted that there is much individual variability in people’s progression through different illness stages, and therefore there is a need to also specify stage modifiers (disease progression factors (e.g. cognitive or neural factors) and extension factors (e.g. physical complications)). Several staging models for eating disorders have been developed. Most of these focus on anorexia nervosa (AN). Criteria for stage differentiation are mostly based on combinations of cognitive, behavioural and physcial features, and illness duration. As yet most of these models are untested. In my talk I will summarise the available evidence on illness stages, stage modifiers and extension factors and their utility in AN and present evidence on what is known about stage-appropriate interventions. I will discuss implications for research and clinical practice.

None Declared

Anorexia nervosa (AN), bulimia nervosa (BN) and Binge Eating Disorders (BED) are diagnosed using the DSM-5 (American Psychiatric Association [APA] 2013) and its revised text (DSM-5-TR; APA 2022) or the ICD-11 (World Health Organization [WHO] 2019). While both systems use a severity indicator for AN based on body mass index (BMI), only the DSM-5 proposes a severity indicator for BN, based on the weekly frequency of purging behaviours, and, in the case of BED, based on the weekly frequency of binge episodes. These severity scores aim to index the level of general and eating disorder (ED) psychopathology, and thus, if valid, should serve as a crucial tool for tailoring treatment decisions, including duration, frequency and type of treatment. However, the current literature is contradictory with regard to the appropriateness of the criteria used and their validity. Therefore, alternative criteria have been proposed (e.g. drive for thinness, duration of the disorder…), especially when exploring chronicity and long-lasting EDs. Furthermore, few studies have directly examined the relationship between severity ratings and treatment outcome. In this presentation, we will discuss current gaps in severity indicators and potential alternatives. Data from existing longitudinal cohorts will be described.

F. Fernandez-Aranda Consultant of: Novo Nordisk. It has no conflict of interest in the current talk. Nothing about pharmacological prescription will be discussed in my talk., S. Jimenez-Murcia Consultant of: Novo Nordisk. It has no conflict of interest in the current talk. Nothing about pharmacological prescription will be discussed in my talk.

The network theory of psychopathology has recently provided a novel view of mental disorders. A growing number of studies employing this methodology has been conducted in eating disorders (ED).

Clinical implications of network approach to ED will be discussed spanning diagnosis and classification, comorbidity, prognosis, and treatment.

Evidence from literature studies and reviews exploring ED psychopathology and treatment through the use of network analysis will be provided. Limitations related to the employment of the network approach will be discussed along with recommendations for future directions.

Overvaluation and concerns about body shape and weight and desire to lose weight are the most central symptoms across patients’ ages and ED diagnoses. Internalizing symptoms, ineffectiveness, and low interoceptive ability play a central role in the psychopathology of ED and promote psychiatric comorbidity. The main issues of network analysis are the selection of network items and the use of cross-sectional data. Prognosis and mechanisms of treatment-induced changes are under-investigated areas.

Network analysis supports a description of ED psychopathology as including eating specific and general psychological symptoms. Treatments designed to improve the most central symptoms and their connections will be essential to explore assumptions of network theory. Longitudinal data from multilevel assessment will allow exploring within person trajectories of psychopathology, observing the dynamic nature of psychopathology and identifying risk and vulnerability factors. This approach will contribute to describe a staging model of EDs, that is essential to improve prognosis formulation and individualize treatment approaches.

None Declared

In Germany there are about 40.000 licensed psychological psychotherapists, 4.000 physicians who work as psychotherapists only, 8.000 psychiatrists who also are specialised in psychotherapy, 4.000 physicians specialised in psychosomatic medicine and psychotherapy, 1.000 physicians of child psychiatry, 35.000 somatic physicians with a training in psychosomatic basic care. This accounts for about 1 therapist for 1.000 inhabitants or 1 per 200 persons with mental problems in ambulatory care. All these therapists are fully reimbursed by health insurance. About 60% of all persons with mental problems have been treated in specialised outpatient psychotherapy.

There are furthermore 900.000 patients per year who are treated for 30 days on average in inpatient departments of psychiatry, psychosomatic medicine and psychotherapy, and another 30.000 patients who are treated in about 300 psychosomatic rehabilitation hospitals for about four weeks.

Given these numbers and costs for psychotherapy, there are multiple regulations for the education and professional practice of therapists. Therapists must undergo three years of training either in cognitive behavior therapy or psychodynamic psychotherapy or systemic psychotherapy, while other forms of psychotherapy, such as Gestalt or Logotherapy are not allowed in training nor patient care. There are detailed requirements in regard to the number of theory lessons, therapeutic self-experience, and treatment with qualified supervision after four sessions. Psychotherapy practice is also restricted to these “scientifically accepted psychotherapies”, which is overseen by two state committees. Depending on the psychotherapy school, health insurance reimburses up to 36 sessions for systemic psychotherapy, 80 for cognitive behavior therapy, 100 for psychodynamic psychotherapy and 300 for analytical psychotherapy.

In summary, psychotherapy in Germany is part of regular patient care and therefore submitted to all respective regulations.

None Declared

Evidence for efficacy of various modalities of psychotherapies is growing and such therapies are increasingly recommended in international guidelines for the treatment of psychiatric disorders. Psychiatrists with strong psychotherapy skills are better positioned to provide individualized and multidisciplinary care. Training in psychotherapy also fosters the development of reflective practice, empathy, and cultural competence, all of which are vital in addressing the diverse needs of patients. Accessibility of psychotherapeutic treatment for the patients can be improved through integrating psychotherapy training in psychiatric training, together with continuous medial education activities. European and other international organisations have published guidelines requiring programs to promote psychotherapeutic competences among psychiatry trainees. However, psychotherapy education and supervision can often become a luxury rather than being a mandatory component of training; and resources are heterogenous. In this presentation, psychotherapy training availabilities and limitations in Turkey will be discussed, with a focus on the psychotherapy courses of Psychiatric Association of Turkey among other initiatives.

None Declared

Childhood maltreatment (CM) encompasses various forms of abuse and neglect before age 18 and frequently manifests in somatic symptoms (SS) such as chronic pain or fatigue. Despite growing recognition of this connection, the relationship between specific CM types and SS, as well as the mechanisms underlying this link, remains incompletely understood.

To examine the current understanding of the association between CM and SS, to highlight gaps in the literature, and propose directions for future research.

A state-of-the-art review searching a range of different databases was performed to explore the interplay between CM (exposure) and SS (outcome) in adults (over age 18).

Identified literature gaps include 1) inconsistency regarding the specific impact of subtypes of CM, specifically of neglect, on the development of SS; 2) narrowing the focus to specific functional syndromes (e.g., fibromyalgia), or selected health outcomes (e.g., respiratory disease) rather than SS as a broad category; and 3) underexploring the impact of culture.

Key recommendations for future research include adopting standardized WHO definitions for CM subtypes, expanding SS diagnostic criteria (e.g. through using comprehensive ICD-11 coding), and integrating cultural moderators (e.g. different health beliefs) into research methodologies. By adopting these recommendations, research could significantly improve patient care and mitigate the broader societal consequences of childhood trauma.

None Declared

Inflammatory processes and innate immune system activation have been implicated in psychiatric disorders. While our prior research highlighted elevated neutrophils, monocytes, and C-reactive protein (CRP) associated with symptom severity in schizophrenia, this study investigates whether similar immune alterations characterize major depression (MD).

Differential blood counts, CRP levels, depression severity (HAMD-21), and psychosocial functioning (GAF) were assessed in controls (n = 129) and patients with first-episode (FEMD: n = 82) or recurrent (RMD: n = 47) MD at hospital admission (T0) and after 6 weeks of treatment (T6). Functional immune parameters, including the phagocytic activity of neutrophils and monocytes, were also measured in a subset of patients with MD (n = 16) and healthy controls (n = 27).

At T0, both FEMD and RMD patients exhibited increased neutrophils (p = 0.034) and CRP levels (FEMD: p < 0.001, RMD: p = 0.021) and decreased eosinophils (FEMD: p = 0.005, RMD: p = 0.004) compared with controls, adjusted for covariates (smoking, BMI, gender). Baseline lymphocyte counts were elevated in RMD (p = 0.003) but not FEMD. Functional analyses revealed significantly increased phagocytic activity of neutrophils in MDD patients compared to controls, both at baseline and T6. Changes in monocyte phagocytic activity correlated with ΔHAMD, indicating a link between immune cell function and symptom improvement.

At T6, eosinophils increased in FEMD (p = 0.011) without significant changes in RMD. Improvement in depression severity correlated with changes in neutrophil counts in FEMD (r = 0.364, p = 0.024). Comparatively, immune alterations in MD showed smaller effect sizes than those observed in schizophrenia. Notably, lymphocyte elevations were specific to recurrent MD, suggesting potential involvement of adaptive immunity in chronic MD.

These findings highlight state- and trait-dependent immune alterations in MD, including heightened neutrophil activity in early stages and adaptive immune involvement in recurrent cases. Functional data further support the role of innate immune activation in MD, with phagocytic activity potentially serving as a biomarker for treatment response. Future studies may inform stage-specific immune-targeted interventions in MD.

None Declared

The search for biomarkers to diagnose depression is an endeavor being pursued in psychiatric research since the 1980s, but hasn’t resulted in clinical application. This remains challenging since the symptomatology of depression is very heterogeneous and because there is no diagnostic gold standard that focuses on an underlying biological mechanism. Despite knowing about the metabolic, endocrine, inflammatory as well as autonomous dysregulation that has been observed in depressed patients, none of these are broadly used to stratify patients. A novel area of research involves the insulin-like growth factor (IGF) system, which plays a vital role in brain development, neurogenesis, and neuroprotection. The insulin-like growth factor (IGF) system, encompassing IGF-I, IGF-II, IGFBPs (1-6), and their receptors, is critical for brain development, neurogenesis, neuroplasticity, and neuroprotection. Insulin-like growth factor binding protein-2 (IGFBP-2), the predominant IGFBP in the central nervous system, regulates IGF-I and IGF-II bioavailability, half-life, localization, and receptor interactions. Serum levels of IGFBP-2 inversely correlate with DTI-derived myelin integrity measures, especially in anterior brain regions.

In a data-driven clustering analysis of a depressed cohort, elevated IGFBP-2 levels delineated a healthier subgroup within a hospitalized cohort of patients with unipolar depression. Additionally we discovered, that patients with higher IGFBP2 levels at inclusion were more likely to remit faster concerning their depressive symptoms, in contrast to an inflammatory marker-defined subgroup. These findings suggest IGFBP-2 as a biomarker for stratifying patients and tailoring interventions in depression. Future research should explore IGFBP-2 and inflammatory markers to better stratify patients and develop targeted therapies, advancing precision medicine for depression and related disorders.

J. Eder: None Declared, P. Falkai Consultant of: Peter Falkai is on the advisory boards of Janssen, Lundbeck, Otsuka, Servier, and Richter, Speakers bureau of: Peter Falkai receives speaker fees from Janssen, Lundbeck, Otsuka, Servier, and Richter

Major depressive disorder is a common, disabling mental disorder characterized by extensive etiological and phenotypic heterogeneity. This heterogeneity makes treatment approaches imprecise and often ineffective. Insight into the underlying biological mechanisms underpinning depression and its subtypes may enable more personalized treatments.

A review of the literature as well as data analyses from 2981 individuals from the Netherlands Study of Depression and Anxiety (NESDA), of whom ˜1900 persons have or lifetime or current Major Depressive Disorder and 650 were healthy controls.

Significant immuno-metabolic dysregulations are present in about 20-30% of people with depression. Such immuno-metabolic depression is characterized by the clustering of 1) atypical, energy-related depressive symptoms such as hypersomnia, fatigue, hyperphagia, and possibly anhedonia, 2) systemic low-grade inflammation with elevated levels of e.g. C-reactive protein, cytokines and glycoprotein acetyls, and 3) metabolic abnormalities involving e.g. obesity, dyslipidaemia, insulin and leptin resistance. Evidence for such clustering is confirmed in large-scale proteomic, metabolomic, gene expression as well as genome-wide data analyses. Persons with immuno-metabolic depression are at a higher risk for cardiometabolic diseases and – from pooled analyses of 4 RCTs in over 1000 individuals - seem to respond less well to standard antidepressant treatment.

Interventions targeting inflammation, metabolism or lifestyle may be more effective treatment options for individuals with immuno-metabolic depression, in line with principles of precision psychiatry.

None Declared

Repeated reports of association of low-grade inflammation in bipolar disorder led to exploration of the causes and consequences of this inflammatory background, now thought to be due to interaction between environmental factors such as infections, stress, pollution, unhealthy life style with immune-genetic background.

Association with functional gene variants of Toll-Like Receptor genes (TLR, NOD), possibly explain diminished response to infections observed in bipolar disorder (rev in Oliveira et al, 2017) association while mitochondrial genes (Angrand et al, BBI, 2021), HLA-E and HLA-G (Boukouaci et al, 2021) contribute to maintenance of inflammation. Association with particular HLA haplotypes very likely explains pro inflammation and auto-immune induction observed particulary in bipolar patients with suicidal behavior and/or with rapid cycling (Tamouza et al, 2020). While HLA haplotypes, in particular when they are associated to anti-inflammatory effect have also been found to be associated with good lithium response (Leclerc et al, 2021).

Systemic inflammation and persistent infections activate different pathways paving the way to biomarker-guided personalized medicine. For example the identification of “autoimmune psychosis” defined by presence of anti-neuronal antibodies in psychosis and in bipolar disorder (Jezequel et al, 2017). Systemic inflammation induced by microbial infection and/or psychosocial factors can also be at the origin of the activation of human endogenous retrovirus (HERV-W) in patients with bipolar disorder (Tamouza et al, 2021). One last example can be found in the immune-metabolic abnormalities that pave the way to metabolic syndrome associated with psychiatric disorders. Various mitochondrial dysfunctions have recently been reported including deregulated bioenergetics and mitochondrial DNA alterations in bipolar disorder, underlying depressive and manic episodes and their association with metabolic syndrome.

Findings accumulated so far favour the consideration of cellular and molecular targets for the treatment of specific subgroups of bipolar disorders. This is the case for clinical trials of the efficacy of anti-inflammatory treatment in patients with blood auto-antibodies against brain receptors. Or for low dose IL-2 therapy in bipolar depression based on the hypothesis that IL-2 is a differentiation factor for T cells and low dose IL-2 combats premature T cell aging and induce the production of new naïve T cells from the thymus particularly T regulator cells (Leboyer et al, 2025). Another example comes from drugs that boost mitochondrial function in bipolar depression (Khandra et al, 2023).

None Declared

The management of dementia presents significant challenges due to the multifaceted nature of major neurocognitive disorders, encompassing cognitive impairments, behavioral and psychological symptoms, and loss of autonomy. Current strategies, including pharmacological and non-pharmacological approaches, have shown limited success, often hindered by adverse effects, lack of efficacy, and insufficient human resources. In this context, emerging technologies offer promising solutions for improving dementia care. Their potential benefits and limitations will be presented: Digital Solutions • Serious Games and Smart Apps: Digital tools can enhance cognitive function and support social engagement for individuals with dementia. Studies show that structured use of these technologies in home settings improves well-being and reduces isolation. Internet of Things (IoT) • Applications: IoT devices such as sensors, GPS trackers, cameras, and wearable technologies are increasingly used to monitor aspects of dementia care. These include activities of daily living (ADLs), sleep patterns, medication adherence, vital signs, and safety concerns like fall detection and wandering.

None Declared

Psychological and behavioural symptoms are an inherent part of neurodegenerative diseases such as Alzheimer’s disease and other dementias or Parkinson’s disease. Despite the growing research on the subject, there are still large gaps in knowledge about their origin, pathophysiology, diagnosis and treatment. In recent years, various initiatives have been carried out in Spain to improve knowledge, especially on the most controversial issues, of various aspects such as Alzheimer’s disease from the point of view of Psychiatry, the use of antipsychotic drugs or depression in neurodegenerative diseases. The presentation will include data on these national initiatives and will address in more detail two studies using Delphi methodology referring to depression in neurodegenerative diseases. The first one addressed depression in the context of Alzheimer’s disease and other dementias in 53 controversial items regarding risk factors, signs and symptoms, diagnosis and treatment. The second one addresses depression in Parkinson’s disease in 49 controversial issues about the aetiopathological mechanisms, clinical features and connections with motor and non-motor symptoms, diagnostic criteria, and therapeutic options. In both cases, in addition to trying to shed light on etiological and clinical aspects, specific advice is provided on the choice of antidepressant treatment and the particularities linked to its prescription.

None Declared

The management of Behavioral and Psychological Symptoms of Dementia (BPSD) remains a key challenge in clinical practice. This presentation will provide an overview of the latest German guidelines, highlighting evidence-based recommendations for pharmacological and non-pharmacological interventions. Key updates emphasize a patient-centered approach, focusing on prevention, risk assessment, and the integration of innovative care strategies. By examining these guideline revisions, the session aims to equip healthcare professionals with practical insights to optimize dementia care and improve patient outcomes in line with current best practices in Germany.

None Declared