Confirmed Symposia

All animals, from insects to humans, share an innate "number sense"—a fundamental ability to perceive quantities that, in humans, forms the foundation of mathematical cognition. Monkeys and crows show neurons tuned to specific numerosities without training, while humans display number discrimination hours after birth. The first talk reveals number-selective neurons in zebrafish larvae from 3 days old and an age-dependent increase in neurons tuned to larger quantities. The second and third talks show spontaneous numerosity perception in humans, influencing behavior, pupil responses, and neural activity. The fourth talk compares neural networks with human data from adults, children, and developmental dyscalculics.

Multiple sclerosis (MS) is cause of chronic neurological disability in patients. The majority of therapeutical approaches for MS are systemic immunosuppressive or immunomodulatory drugs that are not capable to reverse the disease and are able to induce adverse effects. For these reasons, there is a critical necessitate for the development of new treatments thatdecrease the undesired adverse effects and contribute to the return to a best homeostasis. The Symposium will discuss different aspect from preclinical to clinical studies with a translational point of view, to better understand which parameters are relevant for obtaining good pharmacological therapies for MS.

In recent decades, the use of botulinum neurotoxins (BoNT) and other biotoxins has significantly increased in both basic and clinical research. Despite their extensive medical applications, many mechanisms remain poorly understood. This symposium will investigate the mechanisms of BoNT, emphasizing its role in facilitating functional recovery from muscle hyperactivity and its efficacy in chronic pain management. Furthermore, we will showcase how neurotoxins, beyond BoNT, act as versatile biotools for exploring various neurological processes, including axon regeneration and complex neurodisorders like epilepsy and Alzheimer’s disease. These insights will enhance our understanding of their underlying mechanisms and potential therapeutic applications.

Neurodevelopmental disorders (NDDs) are chronic conditions that affect over 1.5% of the global population. Characterized by profound intellectual and physical impairments, these disorders severely impact patients’ functional independence and overall quality of life. While clinical understanding of NDDs has advanced, therapeutic progress is still hindered by limited knowledge of gene regulation, protein functions, and pathophysiological mechanisms. This symposium presents cutting-edge research in NDDs, highlighting preclinical and clinical studies focused on the molecular, cellular, and neural circuit mechanisms that underlie these disorders. We will also explore pharmacological and non-pharmacological approaches for potential treatments, with special emphasis on rare disorders.

Astrocytes, the most abundant glial cells in the central nervous system (CNS), contribute to the pathophysiology of neurological disorders in beneficial or detrimental manners. Modulating astrocytic activity may restore their homeostatic functions or mitigate their harmful dysfunctions, leading to inflammation and excitotoxicity. Understanding the complexity of astrocyte involvement in CNS diseases is fundamental to identify disease-modifying therapies, such as astroglia-targeted gene therapy, in-vivo gene editing or drugs targeting dysfunctional astrocytes. In this symposium, the speakers will present their findings, shaping a scenario involving both the definition of novel roles of astrocytes in the CNS and the development of astrocyte-targeted therapies.

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with various etiologies and heterogenicity in phenotypes. This symposium explores cutting-edge research on genetic, environmental, and molecular mechanisms relevant to ASD and novel therapeutic approaches. Specifically, contributions will investigate how early-life adversity shapes behavioral outcomes in mice with CNTNAP2 suppression (environmental factors, genetic); explore how inflammation and oxidative stress contribute to ASD-related behaviors (protective mechanisms imbalance); examine NEGR1 as possible convergent hub in ASD (genetic convergence); focus on CHD8 suppression phenotypes and introduce SINEUP RNA as an innovative therapeutic strategy for correcting haploinsufficiency-driven neurodevelopmental alterations (genetics, therapy).

The symposium aims at disseminating cutting-edge findings in the development of brain conditioning as a therapeutic strategy for ischemic stroke. The presentations will explore original research about the mechanisms underlying ischemic tolerance, including immune pathways and exosome signalling, being the latter technology a potentially translatable therapeutic strategy. To highlight the therapeutic value of remote ischemic conditioning (RIC), the methodology and results of the first multicenter preclinical trial (TRICS-BASIC) in experimental stroke will be presented. Finally, discussion on the design and preliminary findings from a multicenter randomized phase II clinical trial on RIC in acute stroke patients (TRICS-9) will accomplish the translational paradigm.

Brain-computer interfaces (BCIs) and other emerging neurotechnologies which establish direct communication between the brain and external devices are gaining popularity thanks to the interest of social media and high-profile industry players. These systems have significant future implications in several fields, including medicine and rehabilitation. In addition, BCI experimental paradigms can be leveraged to investigate long-standing questions in Neuroscience, which in turn may lead to further advances in BCIs. Given the speed at which this field is developing, it is essential to foster the scientific debate in order to share the most recent knowledge and pave the way for future applications.

Cerebral cortex complex anatomy derives from a multistep developmental process. The neocortex, specifically, presents a six layered neuronal organization and is divided in different anatomically and functional areas. The secreted glycoprotein Reelin is a key regulator of neocortex cytoarchitecture and function. It is highly expressed by GABAergic and Cajal-Retzius neurons and is involved in many developmental processes: neuronal migration, cortical layers formation, and synaptic plasticity. Reelin is then associated with multiple neurodevelopmental disorders: schizophrenia, bipolar and autism spectrum disorders, epilepsy, and Alzheimer’s. In this symposium we discuss the new discoveries on the role of Reelin in normal and pathological corticogenesis.

Brain complex functions rely on the dynamic interactions with the blood and cerebrospinal fluid (CSF), the proximal environmental fluid that bathes the brain. As a primary regulator of CSF composition, the choroid plexus (ChP) governs interactions at the blood-CSF barrier (B-CSF-B), controlling the body-brain communication axis and influencing development, physiological activity, aging, disease and injury. This symposium explores how ChP signaling shapes the brain using advanced in vivo, ex vivo, and 3D human models. We will highlight the ChP’s integral role across physiological and pathological contexts, offering new insights into its contribution to health and disease.

Hereditary Spastic Paraplegias (HSPs) are a heterogeneous group of monogenic diseases, characterized by the degeneration of the cortico-spinal tract, that altogether affect 2-5 / 100,000 individuals worldwide. No resolutive cure is available for this pathology; novel experimental systems and new therapeutic strategies are therefore an unmet need. In this symposium, we bring together four scientists that study different types of genetic HSPs following different experimental models, i.e., in silico strategies, patient-derived fibroblasts and stem cells, Drosophila melanogaster and Danio rerio. We will provide an overview of the current, most promising strategies to tackle this still uncurable disease.

Treatment-resistant schizophrenia (TRS) is a significant clinical challenge, affecting approximately 30% of patients with schizophrenia. Defined as the persistence of symptoms despite adequate trials of antipsychotic medications, TRS highlights the need for a deeper understanding of its underlying neurobiological mechanisms. Research into molecular, neuroimaging, and neurophysiological signatures is crucial for developing targeted therapies and improving patient outcomes. Identifying these signatures can facilitate better diagnostic criteria and inform treatment strategies, ultimately enhancing the quality of life for individuals suffering from this debilitating condition

Photons are a powerful tool for the minimally invasive control and interrogation of neuronal circuitry in vitro and in vivo. In this symposium we will visit different aspects of the optical techniques available for reporting on the state of single neurons and neuronal circuits and for manipulation of specific cell classes by stimulation of channel rhodopsins with single cell resolution. Here, a broad range of cutting-edge imaging techniques are employed to dissect dysfunctions of vATPases at the synapse, the role of neuro-astrocyte cross talk in spatial memory, brain neuronal network dynamics and all optical modulation of neuronal circuits.

This symposium will discuss innovative findings in the context of Early Life adversities, especially those experienced during the perinatal period, as they have profound implications for maternal well-being, but also for offspring development. We will discuss how maternal adversities, such as exposure to stress or serotonin manipulation are associated with changes in peripheral and central inflammation, gut microbiome and milk composition. A longitudinal cohort of adolescents at high risk for mental disorders will show how alterations in brain morphology and connectivity can mediate the effect of adversities on the onset of clinical outcomes attention deficits and learning difficulties at school.

Environmental stressors present significant challenges to the developing brain. Factors like prenatal drug exposure, early social isolation, and genetic predisposition can lead to enduring neurobehavioral changes associated with long-lasting affective dysregulation. This symposium will bring together leading and emerging researchers to explore how adverse experiences in life disrupt typical brain development trajectories. The aim is to understand the underlying mechanisms of vulnerability to affective diseases, identify potential biomarkers, and eventually develop effective interventions, from prenatal to adult stages, to mitigate the long-term consequences of stress on brain affective health.

Epigenetic mechanisms are critical regulators of nervous system development and function. When compromised, these regulatory mechanisms can have detrimental effects on neurodevelopment and lead to severe brain pathologies, including rare genetic diseases. Today, the advent of epi-drugs opens up new therapeutic opportunities that can be exploited for the treatment of neurodevelopmental disorders. In this respect, a deeper understanding of the epigenetic modulation of neurodevelopment in health and disease is crucial. In the symposium we will present examples of the role of epigenetic control in neurodevelopment using embryonic stem cells, C.elegans, zebrafish and mouse models.

Developmental trajectories shape the critical balance between excitation and inhibition, which is essential for proper neural circuit function and behavior. This symposium will explore the underlying mechanisms of neuronal development at the synaptic, cellular, and network levels, emphasizing their role in neurotransmission and higher-order brain functions. Presentations will showcase recent advances in understanding how neurophysiological changes contributes to both normal brain development and the onset of psychiatric disorders. Using diverse experimental approaches, including rs-fMRI, calcium imaging, and optogenetics, this session aims to provide new insights into the dynamics of excitatory and inhibitory processes underpinning physiological and pathological neural activity.

The symposium aims to integrate the results of a multidisciplinary project that investigated the clinical, molecular, and electrophysiological profiling of Parkinson’s Disease (PD) and the effects of intensive exercise and neuromodulation in patients and animal models of PD (PNRR-MAD-2022-12375804). The preclinical study identified cellular and molecular mechanisms underlying exercise-induced rescue of synaptic plasticity, and behavior and reduction of a-syn spreading. The clinical study provided a link between motor, cognitive, and inflammation-related measures to a-syn species and synaptic plasticity signatures in PD patients. Beneficial effects of non-pharmacological interventions in slowing motor symptom progression were also observed, potentially leading to novel treatments.

Innovative cell replacement therapies using human embryonic stem cells (hESCs) offer promising solutions for nervous system disorders. These approaches harness hESCs’ pluripotency to generate specific neuronal and glial cells for transplantation into damaged regions. Beside some challenges such as immune rejection and optimization of graft composition remain to be addressed, advances including CRISPR-based differentiation protocols and strategies to enhance cell survival and integration into host tissues are currently under investigation to improve the therapeutic effect of the different customized cell products. This symposium will explore these cutting-edge developments, focusing on neurodegenerative diseases and demyelinating disorders as key application areas.

During an injury to the nervous system, intrinsic and extrinsic factors influence axon growth. Neuroinflammation from activated astrocytes and microglial cells hinders regeneration through anti-regenerative molecules such as chondroitin sulfate proteoglycans, semaphorins, and myelin-associated inhibitors. Additionally, mechanical stimuli generated by cell-cell or cell-matrix interactions play key roles in axon regeneration. Nerve repair also requires metabolic adaptation for successful regeneration. This workshop highlights emerging topics and innovative insights into the molecular mechanisms of nerve regeneration, offering guidance for emerging therapeutic strategies.

Serotonergic neurotransmission originating from the Dorsal Raphe Nuclei (DRN) governs a wide repertoire of survival behaviors, shaping emotional responses to stimuli ranging from rewarding to aversive. Cutting-edge technologies that enable monitoring and manipulation of specific neuronal activity as well as profiling single-cell transcriptomic patterns with spatial resolution, are offering unprecedented opportunities to discriminate neural correlates of specific behaviors. This symposium will integrate studies describing DRN functional selectivity at cellular level and studies relating discrete serotonergic projections to specific behaviors. By providing new insights in the functional dissection of serotonergic circuits, we will contribute to the circuit-based understanding of psychiatric illness.

Surviving in social contexts requires the ability to decide about self- and other-related interests. Recent advances have revealed similarities in the neural circuits governing social behaviors across species, from rodents to non-human primates. This symposium will explore how the brain processes and integrates social information to generate other- and self-regarding decisions. We will present cutting-edge studies, using innovative behavioral paradigms, in vivo neurophysiological recordings, and circuit-level manipulation, to investigate how social and neurobiological factors modulate the perception of social cues and guide decision-making. Understanding the neural bases of these behaviors can provide crucial insights into social dysfunction in neuropsychiatric disorders.

Hallucinogens possess unique pharmacological properties, offering both challenges for neuroscience and opportunities for drug development. This symposium explores their molecular mechanisms and therapeutic potential in brain disorders. Presentations include ketamine’s neuroplastic effects in stress, depression (J. Mingardi), and autism spectrum disorder (A. Masi), LSD’s anti-addictive action in alcohol use disorder (D. De Gregorio), and psilocybin’s ability to restore visual function after occipital stroke (S. Comai). Together, these studies highlight hallucinogen-induced neural plasticity and support their evaluation as treatments for psychiatric and neurological disorders, advancing knowledge of brain function and innovative strategies for intervention.

One of the main issues in neurological research is the difficulty of having a realistic model of the disease. In recent years, the advent of new technologies has facilitated the development of innovative cellular tools to study neurological disorders. The aim of this symposium is to present examples of cutting-edge models, such as induced pluripotent stem cells and brain organoids, and to explore their applications, with particular attention on the discovery of pathomechanisms and drug screening. This symposium will highlight the potential of cellular models and provide opportunities to foster new collaborations and synergies among researchers.

In this symposium Dr. Landucci will elucidate the role of cannabinoids in models of cerebral ischemia, epilepsy and Cannabis chronic intoxication. Dr. Scorziello will discuss that (Siah2) E3 ligase activation influences mitochondrial dynamics promoting the degradation of mitochondrial proteins interfering with α-Syn aggregation. Dr. Vinciguerra will show that persistent activation of the cationic channel TRPML1 counteracts neuron loss in ALS and PD, while TPC2 inhibition reduces the infarct volume during cerebral ischemia. Dr. Puente Sanz will discuss the alterations in the expression of the sigma-1 receptor, a chaperone protein that resides at the mitochondria-associated endoplasmic reticulum membranes, in cerebral ischemia.

Memory disruption in CNS disorders involves complex changes affecting different types and phases of memory. Molecular underpinnings of memory collapse are substantially diverse and include a combination of genetic factors, failure of neurotransmitter activity, structural and functional alterations of neuronal circuitry. This symposium brings together emerging experts to discuss recent advances in molecular mechanisms underlying cognitive disruption in neurological and psychiatric disorders. Novel findings on how aberrant neuronal networks develop will be presented, with a focus on the implications for new therapeutic approaches to treat emotional and memory alterations in stress-related disorders, PTSD, schizophrenia, and epilepsy.

Brain energy metabolism has been the object of intense research in recent years. Magistretti highlights lactate dual role in brain metabolism and synaptic plasticity, emphasizing its function as both a fuel and signaling molecule. Paolicelli extends this view, unveiling lactate as a critical metabolic substrate for microglia, essential for synaptic pruning and neuronal maturation, linking disrupted lactate transport to behavioral and developmental defects. Finally, Dell’Anno and Luchinat discuss label-free techniques like MS and NMR, which preserve cellular structure and enable the study of transitions from progenitors to mature neurons, shedding light on the functional and structural changes underpinning this process.

Mitochondrial dysfunction underlies many rare and common diseases, posing significant challenges and therapeutic opportunities. This symposium highlights advances in treating thymidine kinase 2 deficiency, Friedreich ataxia, and mitochondrial optic neuropathies. It will also review ongoing clinical trials, offering insights into current and future directions in mitochondrial medicine. By convening leading researchers and clinicians, the event aims to accelerate translational progress and improve outcomes for patients affected by these debilitating disorders.

Neurodevelopmental disorders (NDDs) are conditions that, by affecting the central nervous system development, cause enduring challenges including language and speech, motor skills, behavioral and cognitive dysfunctions. Despite the identification of hundreds of genetic variants and risk factors (i.e. sex-driven differences) associated with NDDs, the pathogenic molecular mechanisms and putative therapeutic targets are still unidentified. To tackle the NDDs complexity and heterogeneity, a multidisciplinary approach, comprising different experimental models (i.e. 3D-human cellular and animal models) and levels of investigation (i.e. molecular, synaptic and circuit) is needed.

There is an urgent and unmet need for therapies and biomarkers for motor neuron disease (MND), rare disorders characterized by motor neuron degeneration. This panel features four early-career women scientists, based in Canada, USA and Italy, presenting advanced insights in MND research: Dr. Schellino explores cortical neurons involvement in spinal muscular atrophy (SMA), Dr. Petrozziello focuses on tau phosphorylation as a therapeutic target and biomarker for amyotrophic lateral sclerosis (ALS), Dr. Piovesana investigates the neuromuscular junction as source of ALS biomarkers, and Dr. Pozzi introduces a novel antibody-based approach for ALS treatment. Together, they offer diverse insights into MND research.

This symposium aims to present recent advances in unconventional tools, that enable us to interact with neuronal and glial cells at the nanoscale, in the healthy and pathological nervous system. Specifically, we will show how: 1) nano-engineered devices enable modulation of glial cells at different spatio-temporal scale; 2) smart scaffolds employed as nanotransductors can elicit and upregulate cellular functions for nerve regeneration and neuromodulation; 3) extracellular vescicles can be exploited as nanocarriers for RNA therapeutics, targeted via neurotrophin receptors; 4) synthetic or biological nanocarriers can be exploited to deliver therapeutic cargos or to monitor biomarkers in the brain.

Olfaction is the oldest sense in evolutionary terms and a dominant sensory modality in many animals. It plays a fundamental role in the perception of the external environment and guides essential behaviors such as threat avoidance, individual recognition and mating. Olfactory circuits are structurally and functionally highly dynamic, reorganizing daily to update and improve behavioral responses to the ever-changing external olfactory world. The proposed symposium will feature four speakers who will discuss olfactory processing from peripheral to central brain areas, covering topics ranging from mechanisms of odor perception to social behavior in mice.

Neocortical expansion and folding during fetal development are hallmarks of human brain evolution; yet, we are just beginning to unravel the molecular and cellular mechanisms of neocortex development. This symposium will bring together research on neocortical development across model systems, from human organoids and patient samples to rodents. We will focus on radial glia, a key cell type underlying the production and migration of cortical neurons and hence implicated in controlling both neocortical expansion and folding.

Social cognition enhances successful adaptation to complex dynamic environments through mechanisms that support observational learning, problem-solving via social interaction, and emotional recognition. Despite its importance, the neural basis of such processes remains poorly understood, and their disruption contributes to autism-like symptoms in various disorders. This symposium presents recent findings on how the brain implements these mechanisms across different brain areas and cognitive tasks in social and non-social contexts, using a multidisciplinary approach that combines insights from multiple animal models and experimental methodologies. The symposium’s goal is to increase our understanding of the basic and clinical mechanisms involved in social cognition.

Obesity and eating disorders, including anorexia nervosa and binge eating disorder, involve complex disruptions in brain circuits regulating appetite, reward, and emotional processing, as well as hormonal and neurotransmitter imbalances. Investigating these mechanisms offers opportunities to identify novel therapeutic targets. By integrating diverse complementary insights, this symposium aims to advance understanding of the neurobiological bases of obesity and eating disorders, fostering the development of personalized interventions that address both the physiological and psychological aspects of these conditions.

Emerging evidence highlights the critical role of neuroimmune interactions in driving synaptic dysfunction and neuronal network disruption across neurodegenerative diseases, while avoiding and/or resolving CNS inflammation may prevent neuronal damage. Recent developments in these fields will be discussed during the symposium. The first section will analyze the impact of inflammation and the potential of its resolution on synaptic dysfunction and neurodegenerative mechanisms in neurological disorders. The second section will explore new cellular (neutrophils and microglia) and molecular aspects implicated in dysfunctional neuroimmune crosstalks in Alzheimer’s disease and Multiple Sclerosis.

Several neurological diseases are related to imbalances in protein acetylation levels and transcriptional dysfunctions. Notably, the epigenetic erasers HDACs exert their biochemical effects not only on the histone tails but also with non-histone substrates present in other compartments of the neuronal cells. HDAC inhibitors promise as therapeutics in the neurodegenerative diseases such as stroke, ALS and also to block neurocognitive deficits. The scope of this symposium is to discuss the arising novelties in this immature field that could lead to clinical translation. Particularly, the role of specific HDAC/s and their target genes will be analyzed in specific neurological conditions.

Alzheimer's disease is among the most prevalent neurological disorders, impacting the brain at multiple scales, from molecular pathways to whole-brain networks. Early detection of these alterations is critical for effective disease management. Recent advances in neuroscience and neuroengineering have led to the development of innovative techniques for early diagnosis. This symposium will explore the benefits of these state-of-the-art approaches and their potential applications in clinical practice. Key topics will include the use of AI in neural signals analysis, network neuroscience and digital brain twins for the derivation of novel biomarkers and EEG microstates applied to Alzheimer's diagnosis.

Recent advances in neuroscience reveal the crucial role of non-neuronal cell interactions in both healthy and diseased brain, highlighting their impact on myelination, neuroinflammation, and neurogenesis. In pathological conditions such as multiple sclerosis and neurodegenerative diseases, non-neuronal communication is often disrupted earlier than appearance of neuronal death, leading to progressive neurological dysfunction. This symposium will explore the dynamic and reciprocal interactions of astrocytes, microglia, oligodendrocytes and neural stem cells in both physiological and pathological contexts. This will allow to better understand neurodevelopmental disorders and identify novel therapeutic targets for brain diseases involving glia dysfunction, offering exciting possibilities for future treatments.

For a long time, the study of brain development has largely focused on neurons. However, neurons develop concurrently with microglial cells, astrocytes, oligodendrocytes, and vascular cells, which regulate key developmental processes such as neurogenesis, angiogenesis, axonal outgrowth, synaptogenesis, and synaptic pruning. Therefore, it is not surprising that abnormalities in these cells have been found in many neurodevelopmental pathologies, including Autism, Schizophrenia, and 22q11.2 deletion syndrome. Understanding the mechanisms underlying the crosstalk between these cells and neurons during neurodevelopment is thus critical for devising novel therapeutic strategies against neurodevelopmental disorders.

Accumulating evidence over the last decade indicates that monoamine alterations play an important role in the emergence of cognitive impairments and neuropsychiatric symptoms associated to several neurological illnesses. The proposed symposium sheds light on the recent advancement in the field, showing the involvement of monoaminergic neurotransmission dysfunctions in pathologies such as multiple sclerosis and Alzheimer’s disease, as well as in age-related cognitive decline. Ultimately, dissecting the biological underpinnings and brain circuits implicated in these physio-pathological conditions will pave the way for designing early detection and treatment approaches.

Brain states (e.g. sleep and wakefulness) are associated to specific neural activity patterns and information processing capabilities, yet much remains to be understood. The rise of new groundbreaking tools, such as calcium imaging, optogenetics and large-scale electrophysiology, and their integration with emergent models of the human brain, have been pivotal for observing, manipulating and reproducing neuronal activity with unprecedented precision. This simposium aims at reviewing recent advances in the field: in silico, in vitro and in vivo. The aim is to inspire new ideas for unravelling how brain states emerge, evolve and shape neural computations across scales.

Disruption of Ca2+ homeostasis is a common hallmark of neurodegenerative diseases as well as in air pollution-dependent cognitive dysfunction. These alterations often result from impaired communication between Ca2+-storing organelles like mitochondria, endoplasmic reticulum, and lysosomes. Since effective organelles communication is vital for regulating essential cellular processes -such as mitochondrial dynamics, ER/lysosomal activity, and autophagy- any dysfunction can adversely affect cellular homeostasis, contributing to neurodegeneration. This intricate interplay involves Ca2+ channels and related signaling proteins, making their dysregulation a pivotal factor in disease progression. Understanding these pathways may uncover new therapeutic targets to slow or halt neurodegenerative processes.

Mitochondrial dysfunction is considered one of the pathological hallmark of neurodegenerative diseases, such as Parkinson’s (PD), and together with the impairment of the endo-lysosomal-proteasome system create a cellular toxic vicious cycle with the accumulation of aberrant misfolded proteins causing neuronal cell death. Consequently, the use of compounds which could rescue mitochondrial activity has been a long-standing approach. On this topic, recently, G-protein coupled receptors (GPCRs) or some of their truncated variants, which usually are present on the plasma membrane, have been found expressed in the mitochondria, becoming intriguing targets for new pharmacological therapies.

Psychiatric disorders have a complex etiology involving genetic and environmental factors. Among genetic factors, specific polymorphisms in the genes for kynurenine or BDNF pathways have been associated with higher risk for psychiatric disorders. Among environmental factors, stress and use of both natural and synthetic cannabinoids pose a major risk by impacting the development of cortical trajectories. During the symposium, the speakers will describe how the interaction between these factors affects animal behavior but also neurochemistry, neuroplasticity, and epigenetic changes in cortical and subcortical areas.

Neurodevelopmental disorders are characterized by atypical brain development and function, affecting cognition, behavior, and social interactions. This symposium will explore the cutting-edge applications of optical imaging techniques to study cortical dysfunction in autism spectrum disorder. Leading experts will present their latest research on how optical imaging of neural activity can reveal disruptions in cortical circuits underlying sensory processing, social behavior, and cognitive functions. The session will foster interdisciplinary discussion on emerging biomarkers for early diagnosis and therapeutic targets. Attendees will learn how optical imaging can drive new approaches to understanding and treating these complex conditions.

In the last decades, the role of glial cells in maintaining and shaping CNS functions has soundly emerged, while alteration of astrocytes has been reported in different neurodegenerative diseases. Notably, astrocyte activity is finely tuned by intracellular calcium signalling. This symposium will present published and unpublished data to decipher calcium signalling alterations in Alzheimer and Parkinson diseases. In particular, the dissection of calcium signal alteration, the impact of calcium signalling on calcium-sensing protein activity, and cellular proteostasis will be discussed. This comprehensive approach will propose calcium signalling in glial cells as an intriguing target for future treatments of neurodegenerative diseases.

Psychiatric disorders involve significant disruptions in neurocircuit function, affecting critical brain domains such as affectivity, communication, and cognition. Additionally, sensorimotor process impairments are frequently observed. Understanding the behavioral changes and underlying mechanisms in these disorders is essential for developing innovative treatments to improve patient's quality of life. This symposium will explore recent findings on the interplay between affectivity, communication, and sensorimotor function in various animal models of psychiatric disorders, highlighting behavioral outcomes and neurochemical mechanisms.

This symposium explores the retina’s central role in visual perception and behavior. Retinal cell types and computations have been extensively characterized, but only recently directly linked to complex visually guided behaviors. Our speakers will provide insights on innovative strategies to restore retinal function and how limited input can restore visual behaviors. Then, we will hear about pupillary dynamics' influence on retinal binocularity and low-contrast vision. Finally, we will explore visuo-motor pathways through the superior colliculus, specifically, how retinal information is integrated along the dendrites of behaviorally relevant cell types and the emergence of selective attention.

Microglia, the brain's resident immune cells, play a crucial role in circuit refinement during neurodevelopment and constantly patrol the brain surveying for potential threats. When they detect danger, microglia become reactive, engulfing debris and releasing signaling molecules to trigger inflammation, modulate synaptic activity, and foster regeneration. These functions are essential for proper brain development, plasticity, and recovery from injury, but the underlying molecular mechanisms are still poorly understood. In this symposium, we will discuss how microglia shape brain function and repair in rodent and human models, uncovering new therapeutic targets to promote microglial beneficial functions in brain disorders.

Synapses are dynamic and crowded structures crucial for neural information flow and storage. While much is known about synaptic pathophysiology and its behavioral correlations, a complete understanding of structural and signaling changes in both physiological and neurodegenerative conditions remains elusive. In this Symposium, we will present our contributions to this scientific endeavor employing a multi-level approach that encompasses in vitro studies and in vivo analyses, using functional imaging, biochemistry, and genetically encoded tools for subcellular compartment-specific proteomics. We will provide new perspectives on the mechanisms of disease progression to pave the way for innovative treatments aimed at restoring synaptic failure.

Bridging the gap between animal models and human brain complexity is a long-standing challenge of Neuroscience. Recently, routine access to fresh human tissue samples, obtained from therapeutic neurosurgery, became available, enabling detailed analysis of synaptic and network-level activity, particularly in hippocampal and cortical tissue. Combining electrophysiology, imaging, pharmacology, and computational modeling, we are rapidly expanding our understanding of the unique properties of human microcircuits and mechanisms underlying various physiological processes. Importantly, such a multimodal approach also aids the identification of alterations associated with brain disorders, with significant implications for neurophysiology, drug screening, and personalized medicine.

Understanding the impact of early-life insults on neurodevelopment is essential for addressing brain disorders and mental health conditions. Research on early-life challenges, such as inflammation and exposure to environmental factors (e.g. stress, exposure to phytocannabinoids), highlights the neuroplastic changes that might influence the vulnerability to addiction and neurodevelopmental disorders. This symposium will provide an in-depth examination of the mechanisms that define critical periods of neurodevelopmental vulnerability, from gestation to adulthood. These insights might pave the way for innovative therapeutic strategies aimed at preventing the emergence of neurodevelopmental disorders.

Sleep is a complex, multifaceted process essential for physical health, cognitive function, and overall well-being. Central to understanding sleep are its distinct stages, each playing unique roles in maintaining physiological and psychological balance. This symposium unites diverse research perspectives to explore how sleep stages, particularly slow-wave sleep (SWS) and deep sleep, are integral to advancements in wearable technology, neurological recovery, sex-specific cognitive processes, and evolutionary biology. This unified approach not only enhances our comprehension of sleep’s fundamental mechanisms but also inspires interdisciplinary collaborations aimed at optimizing human health in our increasingly complex world.