Paediatric patients with severe diseases awaiting solid organ or haematopoietic stem cell transplantation are known to experience cognitive impairments, particularly in executive functioning. Neuropsychological pre-transplant evaluation serves as a baseline for identifying executive functioning deficits that may affect the medical and psychosocial aspects of care. This is clinically relevant because patients with poorer executive functioning may show decreased adherence to medical treatments, face greater challenges in coping with their illness, and be more likely to require educational adaptations, including curricular or methodological adjustments based on pedagogical criteria.

This study aimed to assess everyday executive functioning in paediatric patients awaiting transplantation using an ecologically valid measure.

A total of 49 patients (59.2% male) aged between 6 and 18 years (M = 11.4, S.D. = 3.5) were recruited from La Paz University Hospital (Madrid, Spain). Patients were awaiting for various types of organ transplants (kidney: 26, heart: 4, lung: 4, hepato-renal: 3, or liver: 2 patients) or haematopoietic stem cells (10 patients). Patients were assessed using the Spanish parent-reported version of the Behavior Rating Inventory of Executive Function, Second Edition (BRIEF-2) with age- and sex-adjusted norms from the Spanish general population. The three BRIEF-2 composite scores were analysed (the Cognitive, Emotional and Behavioral Regulation Indexes), and clinically relevant scores were set at T ≥ 65 points.

Clinically significant levels of executive deficits were observed in 33.3% of patients regarding cognitive regulation problems, in 32.7% regarding emotional regulation difficulties and in 26.5% regarding behavioural regulation problems.

Between 1 in 4 and 1 in 3 patients have shown some type of executive regulation difficulties. The early identification of executive functioning deficits in paediatric transplant candidates is crucial. Incorporating standardised ecologically valid measures, such as the BRIEF-2, into routine assessments can help detect neuropsychological impairments at an early stage, allowing timely therapeutic or preventive interventions (e.g., psychological prehabilitation). This approach can improve medical outcomes and quality of life and guide educational adaptations to support academic performance.

None Declared

Children with Noonan syndrome, the most prevalent RASopathy, exhibit a characteristic neurocognitive phenotype. Specific difficulties in learning, memory, and executive function are among the most frequently observed manifestations documented in the scientific literature.

The present study aimed to measure specific learning difficulties and intelligence in children with RASopathies.

A total sample of 47 patients (55.3% male) aged 3–16 years (M = 8.6, S.D. = 3.1) was recruited from various Spanish regions (Murcia, Alicante, Gandía, Valencia, Castellón de la Plana, Tarragona, Cantabria, Asturias, Zaragoza, Madrid, Badajoz, Huelva, Sevilla and Cádiz), within the framework of The Grey Matter project. Most patients were diagnosed with Noonan syndrome, and some had Cardiofaciocutaneous syndrome. The most frequent mutations were PTPN11 (72.3%), RIT1 (6.4%), and unknown mutations in 12.8% of patients. Patients were assessed using the Spanish version of the Wechsler Preschool and Primary Scale of Intelligence, Fourth Edition (WPPSI-IV) or the Wechsler Intelligence Scale for Children, Fifth Edition (WISC-V) according to age; the Spanish Reading Processes Evaluation Battery (PROLEC) according to the appropriate age range (from 6 years); and the Spanish Writing Processes Evaluation Battery (PROESC), from 8 years.

On the one hand, 32.3% presented with severe difficulty in reading words. In turn, 30% of the children showed severe difficulty in reading comprehension of texts when they were read by an examiner, and 29% after reading by themselves. On the other hand, 56% of the children presented severe orthographic difficulty in writing words and 50% presented severe difficulty in written expressions. Finally, regarding intelligence, the mean total IQ of the children was 84.7 points (S.D. = 15.1), with better scores on the Verbal Comprehension Index (M = 89.4; S.D. = 16), Visual Spatial Index (M = 87.7; S.D. = 13.8), and Fluid Reasoning Index (M = 88.6; S.D. = 11.9), in contrast with the Working Memory Index (M = 84.3; S.D. = 13.2), and the Processing Speed Index (M = 83.2; S.D. = 14.4). In turn, 42.6% of children had low global intelligence scores (IQ ≤ 79).

In conclusion, children with RASopathies, particularly those diagnosed with Noonan syndrome, need educational support to compensate for all these significant academic difficulties.

None Declared

Background: Lifestyle factors are linked to differences in brain aging and risk for Alzheimer’s disease, underscored by concepts like ‘cognitive reserve’ and ‘brain maintenance’. The Resilience Index (RI), a composite of 6 factors (cognitive reserve, physical and cognitive activities, social engagement, diet, and mindfulness) provides such a holistic measure.

This study aims to examine the association of RI scores with cognitive function and assess the mediating role of cortical atrophy.

Baseline data from 113 participants (aged 45+, 68% female) from the Healthy Brain Initiative were included. Life course resilience was estimated with the RI, cognitive performance with Cognivue®, and brain health using a machine learning derived Cortical Atrophy Score (CAS). Mediation analysis probed the relationship between RI, cognitive outcomes, and cortical atrophy.

In age and sex adjusted models, the RI was significantly associated with CAS (β= -0.25, p = 0.006) and Cognivue® scores (β= 0.32, p < 0.001). The RI-Cognivue® association was partially mediated by CAS (β= 0.07; 95% CI [0.02, 0.14]).

Findings revealed that the collective effect of early and late-life lifestyle resilience factors on cognition are partially explained by their association with less brain atrophy. These findings underscore the value of comprehensive lifestyle assessments in understanding the risk and progression of cognitive decline and Alzheimer’s disease in an aging population.

R. Ezzeddine: None Declared, D. Oshea: None Declared, S. Camacho: None Declared, L. Besser: None Declared, M. Tolea: None Declared, J. Galvin Employee of: Cognivue (Chief Scientific Officer of Cognivue). Cognivue devices are used for research conducted at the center., C. Galvin: None Declared, L. Wang: None Declared, G. Gibbs: None Declared

Centropontine myelinolysis (CPM) is an acute demyelinating neurological disorder that primarily affects the central bridge and is frequently associated with rapid correction of hyponatremia. Common clinical manifestations of CPM include spastic quadriparesis, dysarthria, pseudobulbar palsy and encephalopathy of varying degrees. In addition, CPM could be accompanied by neuropsychiatric manifestations, such as personality changes, thymic symptoms, acute psychosis, paranoia, hallucinations or catatonia, usually associated with additional brain damage, described as extrapontine myelinolysis (EPM).

Study the nature of comorbidity between CPM and mood disorders, particularly depression.

We present the case of a patient hospitalized in the psychiatry department B of the Hedi Chaker hospital in Sfax in July 2024. He was been admitted at the request of a third party for behavioral disorders such as agitation and refusal of treatment.

This is Mr. S.BH aged 68, with a psychiatric family history of follow-up for unspecified psychiatric disorders in a niece. He has no psychiatric history, but has a somatic history, unmonitored high blood pressure as well as chronic constipation causing hyponatremia, which was quickly corrected 1 month ago. The latter was responsible for CPM objectified on the brain MRI requested by a free practice neurologist who consulted him for agitation. Our patient is married. He has been retired for a few months and previously worked as a farmer for 35 years. According to the family, the history of his illness dates back to March 2024, following professional stressors when he began to present multiple somatic complaints, with anorexia and weight loss as well as a tendency towards isolation. Since June 2024, following the CPM, he believed that the police wanted to harm him. As a result, he became anxious and agitated. At the interview: Slowed down on the psychomotor level, the contact was superficial, the mood was sad, his speech was provoked, poor and conveyed in a low voice verbalizing anhedonia, he presents congestive disorders and he refuses treatment and diet at the beginning. The patient obtained a score of 12 on < < the Geriatric Depression Scale GDS >> and a score of 12 on < <the mini-mental state examination MMSE >>.

This case demonstrates that depression might represent the main manifestation of CPM, especially in the early stages of the disease, which should be taken into consideration when evaluating patients with acute abnormalities of sodium metabolism.

None Declared

Chronic mental illness is a significant risk factor for developing neurocognitive disorders. Advanced molecular imaging techniques, such as amyloid PET and FDG-PET, provide critical insights into the neurobiological mechanisms that link psychiatry and neurology, enhancing our understanding of the continuum between these fields.

This study aims to describe the clinical history of chronic mental illness in a sample of patients with diagnosis of dementia, using molecular imaging to investigate the relationship between psychiatric history and neurodegenerative pathology.

We conducted a retrospective, descriptive analysis of patients who underwent amyloid PET imaging at the Neurology Department of Infanta Leonor University Hospital from January 2019 to October 2024. Inclusion criteria mandated a documented history of chronic mental illness, irrespective of psychiatric hospitalization. Collected data included demographic variables (age, sex), cardiovascular risk factors, psychiatric diagnoses according to DSM-5, years of mental illness, neurological diagnoses, and results from FDG and amyloid PET imaging. Ethical approval was obtained, and statistical analyses were performed using SPSS 22.0.

A total of 25 patients were included. The main characteristics of the sample are shown in Table 1.

Among those with a chronic mental illness history exceeding ten years (N=8), the diagnostic distribution was as follows: 20% Alzheimer’s disease, 20% Lewy body dementia, 20% major depressive disorder, 10% post-traumatic stress disorder, and 10% indeterminate. Notably, 75% of Alzheimer’s patients and 66.6% of those with Lewy body dementia had a history of major depressive disorder. Patients with frontotemporal dementia often presented with neurocognitive behavioral disorders or obsessive-compulsive disorder. Among four patients with psychiatric hospitalization, only one received a definitive neurological diagnosis (frontotemporal dementia).

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These findings highlight the importance of considering chronic mental illness histories in the cognitive assessment of patients. The neurobiological links between depressive disorders and Alzheimer’s disease emphasize the need for interdisciplinary approaches in clinical practice. Molecular imaging serves as a pivotal tool in refining diagnostic accuracy, complementing both psychiatric and neurological perspectives, and enabling therapeutic strategies to improve patients’ quality of life.

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Hypericin and hyperforin, key secondary metabolites of Hypericum spp., commonly known as St. John’s Wort, are known for their ability to modulate neurotransmitter systems in the mammalian brain. These compounds, which evolved as plant defense chemicals, have significant implications for their interaction with mammalian neurobiology, particularly concerning serotonin, dopamine, and norepinephrine pathways.

This review aims to elucidate the precise molecular mechanisms by which hypericin and hyperforin influence mammalian brain function. The focus is on understanding how these compounds interact with neurotransmitter transporters and receptors, and how these interactions may lead to both therapeutic and adverse neurobiological outcomes.

A comprehensive review of neurobiological and pharmacological literature was conducted, focusing on studies that detail the molecular interactions of hypericin and hyperforin with key components of neurotransmitter systems in mammals. in vitro binding assays, in vivo neuropharmacological studies, and molecular dynamics simulations were reviewed to understand these compounds’ binding affinities, receptor modulation, and downstream signaling effects.

Hypericin, with its planar polycyclic structure, exhibits a strong affinity for serotonin transporters (SERT), where it acts as a non-competitive inhibitor, leading to increased synaptic levels of serotonin. This mechanism mirrors that of selective serotonin reuptake inhibitors (SSRIs) but also introduces the potential for serotonin syndrome when combined with other serotonergic agents. Additionally, hypericin’s ability to generate reactive oxygen species (ROS) under light exposure contributes to neurotoxicity, particularly in regions of the brain exposed to higher oxidative stress.

Hyperforin, characterized by its phloroglucinol core and multiple prenyl groups, exerts its effects primarily through modulation of synaptic vesicle function and ion channel activity. It non-selectively inhibits the reuptake of several neurotransmitters, including serotonin, dopamine, and norepinephrine, through a mechanism involving transient receptor potential (TRP) channels. This broad-spectrum inhibition can lead to significant changes in synaptic plasticity and neurotransmission, impacting mood regulation, anxiety, and cognition.

The interaction of hypericin and hyperforin with mammalian neurotransmitter systems underscores their potential as both therapeutic agents and neurotoxins. The molecular mechanisms by which these compounds modulate neurotransmitter transporters and receptors reveal a delicate balance between beneficial and adverse effects. Understanding these mechanisms is critical for evaluating the safety and efficacy of Hypericum extracts in clinical contexts, particularly regarding their impact on brain function and the potential for neurotoxicity.

None Declared

Patients of depression and psychotic disorders are often troubled by unsatisfactory interpersonal relationships. While an inability to maintain a stable sense of self restricts one’s understanding another’s emotional state, whether disrupted self-versus-other referential processing is a transdiagnostic predictor of increased emotion misreading across diagnostic groups has not been explicated.

We tested whether weakened differential learning between self and other may account for impoversihed emotion recognition accross mood and psychotic disorders.

Inpatients admitted for major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SCZ; ns = 59, 32, and 43) and 40 healthy controls were recruited. Aside from ratings of depressive and schizophrenic symptoms by psychiatrists, participants were assessed on self- versus other- referential learning, emotion recognition, emotion sharing.

Regression analysis indicates lower effectiveness of self-other tagging to be a predictor independent from symptom severity for increased emotion misrecognition across MDD, BD and SCZ (F(8, 160) = 8.52, p < 0.001). Clinical groups showed lower accuracy for other-referential recall and emotion recognition, but comparable emotion sharing and self-prioritization to healthy controls.

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Heightened emotion misrecognition in MDD, CD, and SCZ patients can be traced back to the weakened ability in coordinating self- and other-representations according to task-demands. Future examinations on whether interventions on brain regions pertaining to self-versus-other learning might enhance emotion recognition in different patient groups would be clinically relevant.

None Declared

Atypical antipsychotics (APs) are the drugs of choice for the treatment of the acute episodes and for relapse prevention in schizophrenia (SZ) and psychosis. Nevertheless, these drugs have side effects and particularly increase the risk to develop metabolic syndrome. Moreover, it has been reported that first-episode psychosis (FEP) patients have significant trends to insulin resistance, a higher body mass index and a higher rate of obesity, compared to the healthy subjects. Changes in gut microbiome have been linked to increased systemic inflammation, which could be associated with metabolic disturbances and the development of SZ. In this context, some previous studies have explored the efficacy of probiotic supplementation in SZ, showing benefits in gut regulation and in improving the metabolic effects of APs.

The purpose of this study is to evaluate the effectiveness of an add-on postbiotic to Aps on metabolic disturbances and psychopathological variables in patients diagnosed with FEP or schizophrenia spectrum disorder (SSD). , as well as to determine whether the addition of postbiotics can improve biomarkers related to compensatory immunity and the endocannabinoid system.

A randomized, double-blind, placebo-controlled clinical trial, in which postbiotic or placebo will be administered for 12 weeks as add-on APs. The study comprises two branches: FEP branch, patients recently diagnosed with first psychotic episode; and SSD branch, patients with long-standing psychotic disorder. Five follow-up appointments will be conducted along the 12 weeks to carry on clinical assessments. Patients will be monitoring with a glucose sensor, and blood and microbiota will be analysed.

This is a study protocol that is currently underway. No results are available at this time.

Over the past few decades, it has been abundantly evident how important the human microbiota is to both short-term and long-term human health. In this regard, postbiotics seem to have higher benefitial effects and lower risk than probiotics and they offer a promising approach to improve metabolic disturbances and amelioration of psychopathological symptoms in FEP and SSD patients.

None Declared

Impulsivity implies difficulties in control, leading to non-premeditated actions, and troubles resisting distraction and remaining focused on a goal. It is a transdiagnostic construct that is associated with several disorders, including Attentional Deficit and Hyperactivity Disorder (ADHD), Borderline Personality Disorder and Obsessive-Compulsive Disorder (OCD). It is possible to divide impulsivity between impulsive actions, associated with the ability to inhibit actions, and choice impulsivity, that involves decision-making. It is also common to differentiate between trait impulsivity, that involves more stable characteristics, and state impulsivity, in which the impulsive behavior is more transient.

To investigate the association between action impulsivity as a trait (using self-report measures) and as state (using different level of analysis in a computerized task, i.e., behavioral and neuroimaging measures).

52 university students (mean age = 21.4; standard deviation = 3.33) filled the BIS-11 self-report questionnaires and completed a Stroop-matching/stop-signal task while they had their behavioral and hemodynamic brain activity collected using Functional Near- Infrared Spectroscopy (fNIRS). The Stroop-matching/stop-signal task had three conditions varying the inhibitory demands: Congruent/Unrelated; Incongruent/Unrelated and Incongruent/Related. Spearman correlations were performed between scores of the BIS-11 subscales (Attentional, Motor and Non-planning impulsivity) and the reaction time (RT) and hemodynamic responses (β) of the Stroop-matching/stop-signal task. Alpha level = 0.05.

RTs in all conditions of the task were positively correlated with Motor Impulsivity scores (Congruent/Unrelated, rho = .31, p = .025; Incongruent/Unrelated, rho = .27, p = .049; Incongruent/Related, rho = .38, p = .005). Brain activity in the left temporoparietal region was positively correlated with Attention Impulsivity scores (rho = .29, p = .033).

Motor and attentional aspects of trait impulsivity can be differently correlated with behavioral and neurophysiological measures of state impulsivity. In this study, motor impulsivity was correlated with more peripherical measures of inhibition (reaction times) while attentional impulsivity was correlated with activity in temporoparietal regions commonly associated with inhibition of distractive stimuli. Greater levels of motor and attentional impulsivity were associated with slower responses and greater brain activity, respectively.

None Declared

The lack of accessible plasma biomarkers to identify target populations limits the promise of precision medicine for Alzheimer’s Disease (AD). Amnestic mild cognitive impairment (aMCI) is an important risk for AD and often occurs years before the onset of AD.

Based on an emerging mechanistic model of mitochondrial mechanisms of brain plasticity, we studied the role of acetylcarnitine and free-carnitine levels assayed in plasma as potential markers of cognitive dysfunction in subjects with aMCI or early-AD.

We used available samples from two independent cohorts well characterized for clinical and neuropsychological characteristics together with ultraperformance liquid chromatography-tandem mass spectrometry and computational approaches. Cerebrospinal fluid (CSF) measures of b-amyloid accumulation and t-Tau levels were also available and used in computational modeling.

Within the primary cohort, our data showed decreased levels of carnitine in relation to cognitive function as assessed by using the Mini Mental Status Exam (MMSE) in women but not men with CI as compared to age- and sex-matched HC. Furthermore, the magnitude of carnitine deficiency reflected the severity of cognitive dysfunction in a sex-specific manner (women: p = 0.015; men: p = 0.441). Our data also replicated the prior finding of decreased LAC levels in both women and men with AD, supporting the robustness of the study samples assayed in our new study. Using computational approaches, we found that the integration of these mitochondrial measures with canonical CSF biomarkers improves diagnostic accuracy. A second cohort provides a validation of the sex-specific relationship between free-carnitine deficiency and the severity of cognitive dysfunction.

Taken together with prior mechanistic studies in rodents, the current findings support future research on the development of individualized treatment models targeting sex-specific changes in mitochondrial metabolism.

None Declared

Lewy body dementia (LBD) is characterized by a range of complex neuropsychiatric symptoms that can initially mimic other psychiatric disorders, particularly melancholic depression. Failure to recognize these symptoms can lead to delayed diagnosis and inappropriate management.

This case report highlights the importance of a thorough evaluation of neuropsychiatric symptoms in the diagnosis of Lewy body dementia (LBD).

This case report was compiled through clinical observations, patient history from family members, and medical testing. Literature on LBD was reviewed to assess treatment strategies in light of this patient’s condition.

Mr. T.C., 75 years old, followed for hyperthyroidism and benign prostatic hyperplasia, was admitted for a severe depressive episode with melancholic features. Despite treatment with fluoxetine, mirtazapine, and olanzapine, his clinical condition did not improve. The patient exhibited food refusal, active suicidal ideation, and thoughts of incurability, along with a delusional syndrome. The Mini Mental State Examination (MMSE) revealed cognitive impairment with a score of 21/30. An initial brain MRI showed no abnormalities. The treatment was adjusted with the introduction of paroxetine alongside olanzapine and mirtazapine, but there was no significant improvement. A follow-up brain MRI revealed periventricular vascular leukoencephalopathy and moderate cortical atrophy, directing the diagnosis towards Lewy body dementia. The appearance of additional neuropsychiatric symptoms, including visual hallucinations, cognitive fluctuations, and mild parkinsonian signs, further supported the diagnosis of LBD. Treatment was then adjusted with the introduction of quetiapine, which is better tolerated in the context of LBD due to its favorable therapeutic profile.

This case emphasizes the importance of accurately diagnosing neuropsychiatric disorders in Lewy body dementia. Appropriate management, based on a thorough clinical evaluation, can prevent treatment errors and improve the patient’s quality of life.

None Declared

Using a ‘transdiagnostic’ paradigm for psychopathology, we review the evidence-base for the different treatment interventions for anger, aggression and violence (AAV). We aim to more accurately link the range of psychopathology associated with AAV to underlying brain structures and functional neurocircuitry. Building upon these findings, we propose a working model that may have greater clinical utility than reliance upon a purely ‘disorder-based’ paradigm for addressing AAV. This will permit greater understanding of when anger (which has also conferred evolutionary survival advantages) can become maladaptive and destructive. This comprehensive, ‘interventionist’ model will hopefully lead to better clinical conceptualization of AAV, especially since most AAV presents more commonly in the context of interpersonal/situational stressors and to non-forensically trained clinicians.

1. 1. To identify biological, cognitive, disorder-based, developmental and personality predispositions to AAV

2. 2. To link neuroanatomical and functional brain circuitry with onset and maintainence of AAV

3. 3. To identify how pharmacological and non pharmacological interventions work, and ‘where’ in the brain,

4. 4. To review the evidence-base supporting various treatment interventions

Database review of PUBMED, PsychINFO, Google Scholar and treatment guidelines dating back 15 years (review articles, treatment guidelines, meta-analyses and randomized controlled trials).

This will be visually depicted in an electronic slide (or >1 slide, if permitted) to identify:

1. 1) The inter-relationship between contextal factors, the psychopathology of AAV and undelying brain ‘circutry’

2. 2) The specific nature of the impulsive anger, ‘reactive’ aggression and violence response ‘cycle’ and where in this cycle various interventions can be effectively utlized

3. 3) Which patient populations respond best to which types of interventions

1. 1. AAV are hyperarousal states, with outcomes that can be successfully managed

2. 2. The evidence-base for the role of medications is more limited

3. 3. The evidence-base for the role of various psychotherapies is greater, with specific therapies being particularly useful across psychiatric disorders and populations

4. 4. Psychodynamic approches remain curently underutilized and underappreciated

5. 5. Both medications and therapy influence brain neuroplasticity separately and synergistically

None Declared

Eye-tracking technology is a sensitive and direct method of measuring social-cognitive abilities regardless of language, causing minimal cognitive strain and with the advantage of its passive presentation of stimuli to participants, which allows observation without requiring verbal interaction nor explicit responses.

Our aim was to study variations in social attention among adults diagnosed with ASD, ADHD, comorbid ASD and ADHD, and non-clinical individuals using eye-tracking technology.

We recruited a total of 80 participants over the age of 18 from the Psychiatric External Ward of Vall Hebron University Hospital, resulting in approximately 20 participants in each group. Social attention was assessed using vignettes from the Autism Diagnostic Observation Schedule-2 (ADOS-2).

Preliminary results revealed significant statistical differences among the groups in the variables analyzed, indicating that individuals with ASD display distinct patterns of visual attention toward Areas of Interest (AOIs) containing social information compared to the other groups. No differences were found in the duration of fixation on the characters’ eyes among the groups. However, participants diagnosed with ASD and ASD+ADHD tended to spend more time looking at regions with lower social information density, such as the characters’ hands in the third vignette.

These findings shed light on social attention profiles across clinical and non-clinical populations, indicating specific patterns associated particularly with ASD, and highlight the importance of considering multiple aspects of social cognition. By employing eye-tracking technology, this study provides valuable insights into the underlying mechanisms of social attention across different neurodevelopmental conditions. Furthermore, the lack of significant differences in eye fixation duration on the eyes among clinical groups challenges conventional beliefs regarding social attention deficits in ADHD compared to ASD.

Using objective measures like eye-tracking can enhance our understanding of these complex neurodevelopmental conditions, potentially aiding in diagnosis and guiding the development of targeted interventions to address social cognition challenges in populations with neurodevelopmental disorders.

Our findings may contribute to a better understanding of social attention differences between ASD, ADHD, comorbid ASD+ADHD, and non-clinical individuals, paving the way for the design of more tailored and effective interventions.

None Declared

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease that affects the central nervous system (NP-SLE) in approximately 30-40% of patients, with psychosis being one of the less common yet very serious manifestations, occurring in about 2-3.5% of cases. Diagnosing psychosis in SLE can be challenging, requiring careful integration of medical history with appropriate complementary tests (immunological, CSF, neuroimaging…) while considering other possible differential diagnoses.

To highlight the importance of considering this condition (as well as other rare causes of neuropsychiatric involvement) in patients presenting with atypical psychotic symptoms accompanied by cognitive and behavioral disturbances.

Presentation of a clinical case and literature review.

A 69-year-old female presents with a complex medical history, including melanoma, meningioma, and cerebral microangiopathy. Since 2019, prolonged activated partial thromboplastin time (aPTT) and lupus anticoagulant have been observed. In 2020, she developed neurological symptoms such as blurred vision, diplopia, dizziness, and instability. In December 2022, she consults for depressive symptoms and memory problems. June 2023, she was admitted to Psychiatry ward for a psychotic episode characterized by poorly structured and apparently fluctuating delusional symptoms. There was also evident disorganization, confusion, incoherent behavior, memory deficits, and functional decline. During the hospitalization, her condition initially worsened, with bizarre behaviors fluctuating, requiring mechanical and pharmacological restraint on several occasions. Blood tests showed bicitopenia (leukopenia and thrombocytopenia), along with renal insufficiency. Antiphospholipid syndrome was confirmed. Subsequently, her delusional symptoms remitted, and she was discharged. A second scheduled admission in internal medicine followed for diagnostic clarification during which SLE (ANA+, SSA, SSB, anti U1RNP, anti Sm D, and anti-DNA+) and antiphospholipid syndrome were confirmed. Hydroxychloroquine and anticoagulation (Sintrom) were initiated.

She currently remains under follow-up in both Internal Medicine and Psychiatry with functional, cognitive, and emotional improvement, allowing for the reduction of antipsychotic and antidepressant medication without relapse. A cognitive decline has been ruled out by the dementia unit.

In the case of SLE and its neuropsychiatric manifestations (NP-SLE), there are no specific markers, making detailed medical history, thorough screening, and differential diagnosis essential. Appropriate use of complementary tests and close coordination with other medical specialties are crucial, requiring a multidisciplinary and holistic approach.

None Declared

Bilateral pallidodentate calcinosis (BPC), also known as Fahr’s disease, is an uncommon neurodegenerative disorder that may be either genetic or sporadic. It is distinguished by bilateral and symmetrical deposits of calcium in the basal ganglia and occasionally in the cerebral cortex, impacting the regulation of motor and cognitive functions.

To underline the diagnostic pitfalls faced in Fahr’s disease when psychotic manifestations are predominant, thereby emphasizing the need to integrate neuroimaging and diagnostic assessments in differenciating this disease from a primary psychotic disorder.

We present a rare case of Fahr’s disease with an atypical initial presentation, where the condition was initially misdiagnosed due to predominant psychiatric symptoms.

The patient, a 34-year-old man, displayed significant behavioral disturbances and cognitive decline since the age of 30. Initial psychiatric assessments identified a delusional syndrome, hallucinatory episodes, and psychomotor agitation, leading to a provisional diagnosis of a primary psychotic disorder. However, neuroimaging subsequently revealed bipallidal calcifications characteristic of Fahr’s disease, and further diagnostic evaluations (neurological examinations, a determination of parathyroid hormone (PTH) levels along with a comprehensive calcium-phosphate evaluation) confirmed the condition.The patient was treated symptomatically with second-generation antipsychotics, alongside supportive therapy, resulting in partial symptom alleviation.

This case underscores the challenges of diagnosing Fahr’s disease when psychiatric manifestations predominate, which can delay appropriate diagnosis and treatment. Continuous, multidisciplinary follow-up is essential for optimal management of psychiatric symptoms.

None Declared

Understanding sex differences in brain structure is crucial for advancing personalized medicine. However, the alterations of sex-based neuroanatomical differences during the early phases of mood and psychotic disorders remain largely underexplored.

This study aimed to evaluate neuroanatomical sex-based differences in a healthy cohort and assess potential alterations in clinical populations from the early psychiatric spectrum using a machine learning approach.

For this, we developed a Support Vector Machine (SVM) model trained to classify sex based on grey matter volume from a cohort of healthy controls (HC, n = 521), aged 15 to 40 years. After optimization and cross-validation, the model was applied to three distinct clinical populations from the same age range: individuals at clinical high risk for psychosis (CHR, n =334), those with recent onset psychosis (ROP, n = 351), and those with recent onset depression (ROD, n = 309).

The model achieved a robust balanced accuracy (BAC) of 85.1% (p < .01) in the HC cohort. When applied to the CHR group, the model maintained a BAC of 85.5%, whereas its performance decreased in the ROP (75.8% BAC) and ROD (79.3% BAC) groups. In contrast to previous literature, female participants in the ROP group exhibited a masculinization of brain patterns, while male participants showed no such reversal. In the ROD group, both sexes revealed a slight tendency toward patterns typical of the opposite sex.

These preliminary findings suggest that sex-based neuroanatomical structures remain preserved at high-risk stages but undergo alterations with disorder progression. Future research will investigate the observed performance decline in relation to other phenotypic factors. These findings offer novel insights into sex-specific neurobiological mechanisms underlying psychotic and mood disorders and their early markers.

None Declared

Treatment-resistant schizophrenia patients have the worst clinical outcomes and poor quality of life, despite the administration of clozapine. Currently, the definition of resistance is based on treatment response, but evidence differentiating resistance remains unclear. The dysconnectivity theory suggests that disrupted brain interactions contribute to schizophrenia pathology. Advances in functional and structural neuroimaging allow exploration of connectivity patterns that may characterize treatment-resistant schizophrenia.

This study aimed to describe functional and structural connectivity patterns in schizophrenia patients on clozapine.

Patients taking clozapine (CLZ) or other antipsychotic (nCLZ) were recruited from the Hospital of the Medical School of Ribeirão Preto. Healthy controls (HC) were recruited from the Hospital database. Seventy-seven participants were selected: CLZ = 35, nCLZ = 27, and HC = 27. Functional connectivity (FC) was assessed via resting-state functional magnetic resonance imaging (rs-fMRI) and ROI-to-ROI analysis using the CONN toolbox. Structural connectivity was analyzed with diffusion tensor imaging and tractography using TRACULA toolbox. ANOVA and Tukey test were used for three-group comparisons, and the t-tests for two-group comparisons. Functional analysis was performed with a significance threshold of p < 0.05 and false discovery rate (FDR) set to p < 0.01.

Reduced frontotemporal FC and increased FC in the frontal-occipital were common in CLZ and nCLZ compared to HC. An increased FC between sensorimotor and the cerebellum was notable in CLZ compared to HC. Structural findings included increased axial diffusivity (AD) and mean diffusivity (MD) in 8 of 10 tracts in CLZ compared to HC. The corticospinal tract and inferior longitudinal fasciculus exhibited increased AD and MD in CLZ compared to nCLZ. The cingulum angular bundle showed significantly altered diffusion measures in nCLZ: increased AD, MD, and radial diffusivity (RD), and reduced fractional anisotropy (FA).

This study described a widespread functional and structural dysconnectivity in CLZ, characterized by reduced frontotemporal FC and increased frontal-occipital and sensorimotor–cerebellum FC. Altered AD and MD measures in the corticospinal tract and inferior longitudinal fasciculus were observed in the CLZ. Alterations in AD, MD, RD, and FA measures in the cingulum angular bundle, particularly noted in nCLZ, may be associated with antipsychotic administration. Further studies are necessary to establish whether these dysconnectivity patterns consistently characterize these patient groups.

None Declared

Alzheimer’s disease (AD) is characterized by the abnormal accumulation of amyloid-β and tau proteins. Previous studies have demonstrated that early-onset AD (EOAD) has more rapid and significant tau accumulation compared to late-onset AD (LOAD). Particularly, postmortem analyses have shown greater tau accumulation in the nucleus basalis of Meynert (nbM) in EOAD. However, there is a lack of clinical studies that directly compare tau pathologies in EOAD and LOAD or explore their associations with clinical symptoms.

To evaluate the tau accumulation patterns in the nbM and other brain regions defined by Braak stages (I/II, III/IV, V/VI) in EOAD and LOAD using 18F-florzolotau PET imaging. Additionally, to analyze the relationship between tau accumulation in the nbM and cognitive function.

The study included 38 amyloid-positive AD patients (15 EOAD, 23 LOAD) and 46 healthy controls (HCs). PET scans with 18F-florzolotau were performed, and the standardized uptake value ratios (SUVRs) of tau accumulation in the nbM and Braak stage regions were calculated using the cerebellum as the reference. Cognitive assessments were conducted using the Mini-Mental State Examination (MMSE) and other neuropsychological tests. Postmortem brain tissue from six AD patients and two HCs was histologically analyzed to validate PET findings.

EOAD patients showed significantly higher tau accumulation in the nbM than LOAD patients (p = 0.004). The SUVRs in Braak stage regions also tended to be higher in EOAD (I/II: p = 0.244, III/IV: p = 0.120, V/VI: p = 0.079). Correlation analysis revealed no significant relationship between nbM SUVR and Braak stage SUVRs in EOAD, whereas LOAD patients exhibited positive correlations in Braak stages I/II (r = 0.50, p = 0.014) and III/IV (r = 0.43, p = 0.043). In LOAD, nbM tau accumulation correlated negatively with MMSE scores (r = -0.55, p = 0.006). In EOAD, higher Braak stage tau was associated with a stronger negative trend in MMSE (III/IV: r = -0.37, p = 0.178; V/VI: r = -0.41, p = 0.126). Histopathological examination confirmed the presence of ghost tangles in advanced AD and intracellular tau in early-stage AD, supporting the PET imaging results.

The study highlights distinct tau pathology differences in the nbM and their impact on cognitive function between EOAD and LOAD. The findings suggest that while nbM tau pathology in LOAD is linked to disease severity, EOAD is influenced more by cortical tau pathology. PET imaging of tau provides a promising approach for enhancing diagnostic and therapeutic strategies for Alzheimer’s disease.

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Cerebrovascular diseases, including white matter hyperintensities (WMLs), are the leading cause of functional disability and comorbid depression. Accurate and timely detection of WMLs is crucial for understanding their pathophysiology, progression, and treatment outcomes of both vascular and depressive symptomatology. Recent advancements in artificial intelligence (AI) and machine learning have facilitated the development of automatic WML detection methods, enhancing efficacy and accuracy in quantifying, localising, and evaluating lesion characteristics.

The aim of this pilot study was to propose the framework for training set of low-shot medical image data in cerebrovascular disease and comorbid depression as novel artificial intelligence (AI) neuroimaging techniques, combined with quantitative measurements can be used to investigate and understand the implications of WMLs on brain structure and function.

We included 25 subjects, 15 with WMLs and 10 controls. Depressive symptoms were assessed by psychiatrist using Hamilton Depression Rating Scale (HDRS) and clinical interview. The neuroimaging data were collected from Magnetic Resonance Department University Clinical Center, Medical faculty, University of Belgrade, Serbia. All images were aligned with MNI space to normalize their intensity. Manual delineation and brain segmentation was performed with 3D slicer software using structural T1v and T2FLAIR images. Statistical analysis was performed to determine the correlation of lesion volume with the total brain volume (TBV) and to compare the TBV in patients with lesions and controls, in an effort to find possible morphometric correlates that may aid in automatic lesion detection and predicting the spacial pattern of WMLs.

Adding to the proposed framework, we have investigated statistical correlates in subjects with WMLs and controls. A statistical analysis was conducted to compare TBV in subjects with WMLs and controls and correlation between WML volume and TBV. The significance of the observed differences is determined, providing insights into the impact of WMLs on TBV.

The average WML volume was 197±154.18 mm3, with the smallest volume measured at 28.92 mm3 and the largest at 552.8 mm3. A significant difference in TBV was observed between patients with WMLs and controls (p-value=0.00216, p<0.05), and a weak negative correlation was found between WML volume and TBV (ρ=–0.167).

Our findings demonstrate reduced TBV in patients with WMLs and depression and emphasize the importance of considering parameters such as TBV in evaluating WMLs. Assessing the impact of WMLs on TBV can provide valuable insights into the progression and severity of cognitive decline and functional impairment but also impact on training dataset preprocessing preparation for AI framework on low shot medical images in cerebrovascular disease.

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There is a growing evidence that a presence of mild behavioral impairment (MBI) in geriatric patients with mild cognitive impairment (MCI) increases the risk of Alzheimer disease. However, neurobiological patterns underling such additional risk remains unclear.

We aimed to investigate structural cortical patterns in MCI patients that differentiate converters from non-converters to Alzheimer disease (AD) and to explore correlations of such patterns with mild behavioral impairment.

Thirty five right-handed geriatric patients with amnestic type of MCI (aMCI) were followed up during the period of 11.3±6.9 months and divided into converters to AD (n=11, mean age 74.6±7.5, 10 females) and non-converters (n=24, mean age 72.6±8.1, 18 females). Patients and matched healthy controls (n=17, mean age 72.3±7.2 years, 14 females) underwent structural 3T MRI at baseline. MRI images were processed via FreeSurfer 6.0 to quantify gray matter thickness for 68 cortical areas according to Desikan atlas. Cognitive status was assessed using the Montreal Cognitive Assessment (MoCA) scale, and the severity of mild behavioral impairment was assessed using the MBI-C (Mild Behavioral Impairment Checklist) at baseline.

Cortical thickness in the left inferior parietal lobe (IPL) and left middle temporal gyrus (MTG) were decreased in converters compared to both non-converters (IPL: F(1,30)=12.8, p=0.0012, Cohen’s d=−1.30; MTG: F(1,30)=12.8, p=0.0012; Cohen’s d=−1.30) and healthy controls (IPL: F(1,24)=11.4, p=0.0025, Cohen’s d=−1.33; MTG: F(1,24)=8.3, p=0.008; Cohen’s d=−1.15) (Image 1A,B).

Converters also showed larger baseline MBI-C scores compared to non-converters (13.8±12.0 vs 7.8±6.6; GML t=2.1, p=0.045) and no difference in baseline MoCA (21.8±4.0 vs 23.2±2.8; GML t=−1.4, p=0.19).

Baseline MBI-C scores in the whole aMCI group correlated negatively with cortical thickness both in the left IPL (R=−0.53, p=0.0011) and left MTG (R=−0.48, p=0.004) (Image 1C). No correlations between MoCA scores and cortical thickness were observed.

Image 1. A: Clusters of decreased cortical thickness according to atlas of Desikan et al. (2006) in converters compared to non-converters and healthy controls. B: Box-plots of cortical thickness in the left inferior parietal lobe and left middle temporal gyrus. C: Scatter plots of MBI-C scores and gray matter thickness in the left inferior parietal lobe and left middle temporal gyrus in the whole aMCI group (n = 35).

Image 1:

The findings suggest that the decreased baseline cortical thickness in the left inferior parietal lobe and middle temporal gyrus with associated greater severity of mild behavioral impairment could be potential marker of increased risk of conversion to AD in aMCI patients.

The study was supported by RSF grant 24-15-00220

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