autism

Organization of thalamic networks and mechanisms of dysfunction in schizophrenia and autism

Thalamic networks, at the core of thalamocortical and thalamosubcortical communications, underlie processes of perception, attention, memory, emotions, and the sleep-wake cycle, and are disrupted in mental disorders, including schizophrenia and autism. However, the underlying mechanisms of pathology are unknown. I will present novel evidence on key organizational principles, structural, and molecular features of thalamocortical networks, as well as critical thalamic pathway interactions that are likely affected in disorders. This data can facilitate modeling typical and abnormal brain function and can provide the foundation to understand heterogeneous disruption of these networks in sleep disorders, attention deficits, and cognitive and affective impairments in schizophrenia and autism, with important implications for the design of targeted therapeutic interventions

The Unconscious Eye: What Involuntary Eye Movements Reveal About Brain Processing

Genetic and epigenetic underpinnings of neurodegenerative disorders

Pluripotent cells, including embryonic stem (ES) and induced pluripotent stem (iPS) cells, are used to investigate the genetic and epigenetic underpinnings of human diseases such as Parkinson’s, Alzheimer’s, autism, and cancer. Mechanisms of somatic cell reprogramming to an embryonic pluripotent state are explored, utilizing patient-specific pluripotent cells to model and analyze neurodegenerative diseases.

Rett syndrome, MECP2 and therapeutic strategies

The development of the iPS cell technology has revolutionized our ability to study development and diseases in defined in vitro cell culture systems. The talk will focus on Rett Syndrome and discuss two topics: (i) the use of gene editing as an approach to therapy and (ii) the role of MECP2 in gene expression (i) The mutation of the X-linked MECP2 gene is causative for the disease. In a female patient, every cell has a wt copy that is, however, in 50% of the cells located on the inactive X chromosome. We have used epigenetic gene editing tools to activate the wt MECP2 allele on the inactive X chromosome. (ii) MECP2 is thought to act as repressor of gene expression. I will present data which show that MECP2 binds to Pol II and acts as an activator for thousands of genes. The target genes are significantly enriched for Autism related genes. Our data challenge the established model of MECP2’s role in gene expression and suggest novel therapeutic approaches.

SWEBAGS conference 2024: The involvement of the striatum in autism spectrum disorder

Beyond Homogeneity: Characterizing Brain Disorder Heterogeneity through EEG and Normative Modeling

Electroencephalography (EEG) has been thoroughly studied for decades in psychiatry research. Yet its integration into clinical practice as a diagnostic/prognostic tool remains unachieved. We hypothesize that a key reason is the underlying patient's heterogeneity, overlooked in psychiatric EEG research relying on a case-control approach. We combine HD-EEG with normative modeling to quantify this heterogeneity using two well-established and extensively investigated EEG characteristics -spectral power and functional connectivity- across a cohort of 1674 patients with attention-deficit/hyperactivity disorder, autism spectrum disorder, learning disorder, or anxiety, and 560 matched controls. Normative models showed that deviations from population norms among patients were highly heterogeneous and frequency-dependent. Deviation spatial overlap across patients did not exceed 40% and 24% for spectral and connectivity, respectively. Considering individual deviations in patients has significantly enhanced comparative analysis, and the identification of patient-specific markers has demonstrated a correlation with clinical assessments, representing a crucial step towards attaining precision psychiatry through EEG.

In vivo scalable investigation of gene functions in the brain

Investigating dynamiCa++l mechanisms underlying cortical development and disease

Contrasting developmental principles of human brain development and their relevance to neurodevelopmental disorders

Perception in Autism: Testing Recent Bayesian Inference Accounts

Investigating activity-dependent processes during cortical neuronal assembly in development and disease

Genomic investigation of sex-differential neurodevelopment and risk for autism

Metabolic Remodelling in the Developing Forebrain in Health and Disease

Little is known about the critical metabolic changes that neural cells have to undergo during development and how temporary shifts in this program can influence brain circuitries and behavior. Motivated by the identification of autism-associated mutations in SLC7A5, a transporter for metabolically essential large neutral amino acids (LNAAs), we utilized metabolomic profiling to investigate the metabolic states of the cerebral cortex across various developmental stages. Our findings reveal significant metabolic restructuring occurring in the forebrain throughout development, with specific groups of metabolites exhibiting stage-specific changes. Through the manipulation of Slc7a5 expression in neural cells, we discovered an interconnected relationship between the metabolism of LNAAs and lipids within the cortex. Neuronal deletion of Slc7a5 influences the postnatal metabolic state, resulting in a shift in lipid metabolism and a cell-type-specific modification in neuronal activity patterns. This ultimately gives rise to enduring circuit dysfunction.

Freeze or flee ? New insights from rodent models of autism

Individuals afflicted with certain types of autism spectrum disorder often exhibit impaired cognitive function alongside enhanced emotional symptoms and mood lability. However, current understanding of the pathogenesis of autism and intellectual disabilities is based primarily on studies in the hippocampus and cortex, brain areas involved in cognitive function. But, these disorders are also associated with strong emotional symptoms, which are likely to involve changes in the amygdala and other brain areas. In this talk I will highlight these issues by presenting analyses in rat models of ASD/ID lacking Nlgn3 and Frm1 (causing Fragile X Syndrome). In addition to identifying new circuit and cellular alterations underlying divergent patterns of fear expression, these findings also suggest novel therapeutic strategies.

Translational Research in Tuberous Sclerosis as a Model for Autism and Epilepsy

Therapeutic Strategies for Autism: Targeting Three Levels of the Central Dogma of Molecular Biology with a Focus on SYNGAP1

Mechanisms of human cortical development and neuropsychiatric disease

Precision Genomics in Neurodevelopmental Disorders

Expanding the role of MAST kinases in brain development and epilepsy: identification of de novo pathogenic variants in MAST4

Myelin Formation and Oligodendrocyte Biology in Epilepsy

Epilepsy is one of the most common neurological diseases according to the World Health Organization (WHO) affecting around 70 million people worldwide [WHO]. Patients who suffer from epilepsy also suffer from a variety of neuro-psychiatric co-morbidities, which they can experience as crippling as the seizure condition itself. Adequate organization of cerebral white matter is utterly important for cognitive development. The failure of integration of neurologic function with cognition is reflected in neuro-psychiatric disease, such as autism spectrum disorder (ASD). However, in epilepsy we know little about the importance of white matter abnormalities in epilepsy-associated co-morbidities. Epilepsy surgery is an important therapy strategy in patients where conventional anti-epileptic drug treatment fails . On histology of the resected brain samples, malformations of cortical development (MCD) are common among the epilepsy surgery population, especially focal cortical dysplasia (FCD) and tuberous sclerosis complex (TSC). Both pathologies are associated with constitutive activation of the mTOR pathway. Interestingly, some type of FCD is morphological similar to TSC cortical tubers including the abnormalities of the white matter. Hypomyelination with lack of myelin-producing cells, the oligodendrocytes, within the lesional area is a striking phenomenon. Impairment of the complex myelination process can have a major impact on brain function. In the worst case leading to distorted or interrupted neurotransmissions. It is still unclear whether the observed myelin pathology in epilepsy surgical specimens is primarily related to the underlying malformation process or is just a secondary phenomenon of recurrent epileptic seizures creating a toxic micro-environment which hampers myelin formation. Interestingly, mTORC1 has been implicated as key signal for myelination, thus, promoting the maturation of oligodendrocytes . These results, however, remain controversial. Regardless of the underlying pathophysiologic mechanism, alterations of myelin dynamics, depending on their severity, are known to be linked to various kinds of developmental disorders or neuropsychiatric manifestations.

Cell-type specific alterations underpinning convergent ASD phenotypes in PACS1 neurodevelopmental disorder

Children-Agent Interaction For Assessment and Rehabilitation: From Linguistic Skills To Mental Well-being

Socially Assistive Robots (SARs) have shown great potential to help children in therapeutic and healthcare contexts. SARs have been used for companionship, learning enhancement, social and communication skills rehabilitation for children with special needs (e.g., autism), and mood improvement. Robots can be used as novel tools to assess and rehabilitate children’s communication skills and mental well-being by providing affordable and accessible therapeutic and mental health services. In this talk, I will present the various studies I have conducted during my PhD and at the Cambridge Affective Intelligence and Robotics Lab to explore how robots can help assess and rehabilitate children’s communication skills and mental well-being. More specifically, I will provide both quantitative and qualitative results and findings from (i) an exploratory study with children with autism and global developmental disorders to investigate the use of intelligent personal assistants in therapy; (ii) an empirical study involving children with and without language disorders interacting with a physical robot, a virtual agent, and a human counterpart to assess their linguistic skills; (iii) an 8-week longitudinal study involving children with autism and language disorders who interacted either with a physical or a virtual robot to rehabilitate their linguistic skills; and (iv) an empirical study to aid the assessment of mental well-being in children. These findings can inform and help the child-robot interaction community design and develop new adaptive robots to help assess and rehabilitate linguistic skills and mental well-being in children.

Hormonal control of brain sex differences

How do Astrocytes Sculpt Synaptic Circuits?

From symptoms to circuits in Fragile X syndrome

The impact of emerging technologies and methods on the interpretation of genetic variation in autism and fetal genomics

Self-direction in daily stress management: the solution for mental health issues

In the lecture Yvette Roke and Jamie Hoefakker will discuss the positive and negative effects of daily stress on mental health. They will also highlight which characteristics are likely to cause more stress related issues, and why recovery time is very important. They will give an understanding of autism spectrum disorder (ASD) in relation to daily stress and they will discuss the app, SAM the stress autism mate, developed and investigated (SCED design) in co-creation with their patients with ASD.

Dysregulated Translation in Fragile X Syndrome

Baby steps to breakthroughs in precision health in neurodevelopmental disorders

Myelin Formation and Oligodendrocyte Biology in Epilepsy

Epilepsy is one of the most common neurological diseases according to the World Health Organization (WHO) affecting around 70 million people worldwide [WHO]. Patients who suffer from epilepsy also suffer from a variety of neuro-psychiatric co-morbidities, which they can experience as crippling as the seizure condition itself. Adequate organization of cerebral white matter is utterly important for cognitive development. The failure of integration of neurologic function with cognition is reflected in neuro-psychiatric disease, such as autism spectrum disorder (ASD). However, in epilepsy we know little about the importance of white matter abnormalities in epilepsy-associated co-morbidities. Epilepsy surgery is an important therapy strategy in patients where conventional anti-epileptic drug treatment fails . On histology of the resected brain samples, malformations of cortical development (MCD) are common among the epilepsy surgery population, especially focal cortical dysplasia (FCD) and tuberous sclerosis complex (TSC). Both pathologies are associated with constitutive activation of the mTOR pathway. Interestingly, some type of FCD is morphological similar to TSC cortical tubers including the abnormalities of the white matter. Hypomyelination with lack of myelin-producing cells, the oligodendrocytes, within the lesional area is a striking phenomenon. Impairment of the complex myelination process can have a major impact on brain function. In the worst case leading to distorted or interrupted neurotransmissions. It is still unclear whether the observed myelin pathology in epilepsy surgical specimens is primarily related to the underlying malformation process or is just a secondary phenomenon of recurrent epileptic seizures creating a toxic micro-environment which hampers myelin formation. Interestingly, mTORC1 has been implicated as key signal for myelination, thus, promoting the maturation of oligodendrocytes . These results, however, remain controversial. Regardless of the underlying pathophysiologic mechanism, alterations of myelin dynamics, depending on their severity, are known to be linked to various kinds of developmental disorders or neuropsychiatric manifestations.

Counteracting epigenetic mechanisms in autism spectrum disorders

Sleep, development and chromatin regulation in autism

Functional and translational implications of A-to-I editing in brain development and neurodevelopmental disorders

Exploring the endocannabinoid system for intervention innovation in autism

CANCELLED

Don't forget the gametes: Neurodevelopmental pathogenesis starts in the sperm and egg

Proper development of the nervous system depends not only on the inherited DNA sequence, but also on proper regulation of gene expression, as controlled in part by epigenetic mechanisms present in the parental gametes. In this presentation an internationally recognized research advocate explains why researchers concerned about the origins of increasingly prevalent neurodevelopmental disorders such as autism and attention deficit hyperactivity disorder should look beyond genetics in probing the origins of dysregulated transcription of brain-related genes. The culprit for a subset of cases, she contends, may lie in the exposure history of the parents, and thus their germ cells. To illustrate how environmentally informed, nongenetic dysfunction may occur, she focuses on the example of parents' histories of exposure to common agents of modern inhalational anesthesia, a highly toxic exposure that in mammalian models has been seen to induce heritable neurodevelopmental abnormality in offspring born of exposed germline.

Studying genetic overlap between ASD risk and related traits: From polygenic pleiotropy to disorder-specific profiles

Untitled Seminar

Molecular Logic of Synapse Organization and Plasticity

Connections between nerve cells called synapses are the fundamental units of communication and information processing in the brain. The accurate wiring of neurons through synapses into neural networks or circuits is essential for brain organization. Neuronal networks are sculpted and refined throughout life by constant adjustment of the strength of synaptic communication by neuronal activity, a process known as synaptic plasticity. Deficits in the development or plasticity of synapses underlie various neuropsychiatric disorders, including autism, schizophrenia and intellectual disability. The Siddiqui lab research program comprises three major themes. One, to assess how biochemical switches control the activity of synapse organizing proteins, how these switches act through their binding partners and how these processes are regulated to correct impaired synaptic function in disease. Two, to investigate how synapse organizers regulate the specificity of neuronal circuit development and how defined circuits contribute to cognition and behaviour. Three, to address how synapses are formed in the developing brain and maintained in the mature brain and how microcircuits formed by synapses are refined to fine-tune information processing in the brain. Together, these studies have generated fundamental new knowledge about neuronal circuit development and plasticity and enabled us to identify targets for therapeutic intervention.

Clinical neuroscience and the heart-brain axis (BACN Mid-career Prize Lecture 2021)

Cognitive and emotional processes are shaped by the dynamic integration of brain and body. A major channel of interoceptive information comes from the heart, where phasic signals are conveyed to the brain to indicate how fast and strong the heart is beating. This talk will discuss how interoceptive processes operate across conscious and unconscious levels to influence emotion and memory. The interoceptive channel is disrupted in distinct ways in individuals with autism and anxiety. Selective interoceptive disturbance is related to symptomatology including dissociation and the transdiagnostic expression of anxiety. Interoceptive training can reduce anxiety, with enhanced interoceptive precision associated with greater insula connectivity following targeted interoceptive feedback. The discrete cardiac effects on emotion and cognition have broad relevance to clinical neuroscience, with implications for peripheral treatment targets and behavioural interventions.

How are nervous systems remodeled in complex metazoans?

Early in development the nervous system is constructed with far too many neurons that make an excessive number of synaptic connections.  Later, a wave of neuronal remodeling radically reshapes nervous system wiring and cell numbers through the selective elimination of excess synapses, axons and dendrites, and even whole neurons.  This remodeling is widespread across the nervous system, extensive in terms of how much individual brain regions can change (e.g. in some cases 50% of neurons integrated into a brain circuit are eliminated), and thought to be essential for optimizing nervous system function.  Perturbations of neuronal remodeling are thought to underlie devastating neurodevelopmental disorders including autism spectrum disorder, schizophrenia, and epilepsy.  This seminar will discuss our efforts to use the relatively simple nervous system of Drosophila to understand the mechanistic basis by which cells, or parts of cells, are specified for removal and eliminated from the nervous system.

Neural Circuit Dysfunction along the Gut/Brain Axis in zebrafish models of Autism Spectrum Disorder

Reversing autism-related phenotypes in human brain organoids

The Synaptome Architecture of the Brain: Lifespan, disease, evolution and behavior

The overall aim of my research is to understand how the organisation of the synapse, with particular reference to the postsynaptic proteome (PSP) of excitatory synapses in the brain, informs the fundamental mechanisms of learning, memory and behaviour and how these mechanisms go awry in neurological dysfunction. The PSP indeed bears a remarkable burden of disease, with components being disrupted in disorders (synaptopathies) including schizophrenia, depression, autism and intellectual disability. Our work has been fundamental in revealing and then characterising the unprecedented complexity (>1000 highly conserved proteins) of the PSP in terms of the subsynaptic architecture of postsynaptic proteins such as PSD95 and how these proteins assemble into complexes and supercomplexes in different neurons and regions of the brain. Characterising the PSPs in multiple species, including human and mouse, has revealed differences in key sets of functionally important proteins, correlates with brain imaging and connectome data, and a differential distribution of disease-relevant proteins and pathways. Such studies have also provided important insight into synapse evolution, establishing that vertebrate behavioural complexity is a product of the evolutionary expansion in synapse proteomes that occurred ~500 million years ago. My lab has identified many mutations causing cognitive impairments in mice before they were found to cause human disorders. Our proteomic studies revealed that >130 brain diseases are caused by mutations affecting postsynaptic proteins. We uncovered mechanisms that explain the polygenic basis and age of onset of schizophrenia, with postsynaptic proteins, including PSD95 supercomplexes, carrying much of the polygenic burden. We discovered the “Genetic Lifespan Calendar”, a genomic programme controlling when genes are regulated. We showed that this could explain how schizophrenia susceptibility genes are timed to exert their effects in young adults. The Genes to Cognition programme is the largest genetic study so far undertaken into the synaptic molecular mechanisms underlying behaviour and physiology. We made important conceptual advances that inform how the repertoire of both innate and learned behaviours is built from unique combinations of postsynaptic proteins that either amplify or attenuate the behavioural response. This constitutes a key advance in understanding how the brain decodes information inherent in patterns of nerve impulses, and provides insight into why the PSP has evolved to be so complex, and consequently why the phenotypes of synaptopathies are so diverse. Our most recent work has opened a new phase, and scale, in understanding synapses with the first synaptome maps of the brain. We have developed next-generation methods (SYNMAP) that enable single-synapse resolution molecular mapping across the whole mouse brain and extensive regions of the human brain, revealing the molecular and morphological features of a billion synapses. This has already uncovered unprecedented spatiotemporal synapse diversity organised into an architecture that correlates with the structural and functional connectomes, and shown how mutations that cause cognitive disorders reorganise these synaptome maps; for example, by detecting vulnerable synapse subtypes and synapse loss in Alzheimer’s disease. This innovative synaptome mapping technology has huge potential to help characterise how the brain changes during normal development, including in specific cell types, and with degeneration, facilitating novel pathways to diagnosis and therapy.

From the cell biology of synaptic plasticity to SFARI

Mapping the Dynamics of the Linear and 3D Genome of Single Cells in the Developing Brain

Three intimately related dimensions of the mammalian genome—linear DNA sequence, gene transcription, and 3D genome architecture—are crucial for the development of nervous systems. Changes in the linear genome (e.g., de novo mutations), transcriptome, and 3D genome structure lead to debilitating neurodevelopmental disorders, such as autism and schizophrenia. However, current technologies and data are severely limited: (1) 3D genome structures of single brain cells have not been solved; (2) little is known about the dynamics of single-cell transcriptome and 3D genome after birth; (3) true de novo mutations are extremely difficult to distinguish from false positives (DNA damage and/or amplification errors). Here, I filled in this longstanding technological and knowledge gap. I recently developed a high-resolution method—diploid chromatin conformation capture (Dip-C)—which resolved the first 3D structure of the human genome, tackling a longstanding problem dating back to the 1880s. Using Dip-C, I obtained the first 3D genome structure of a single brain cell, and created the first transcriptome and 3D genome atlas of the mouse brain during postnatal development. I found that in adults, 3D genome “structure types” delineate all major cell types, with high correlation between chromatin A/B compartments and gene expression. During development, both transcriptome and 3D genome are extensively transformed in the first month of life. In neurons, 3D genome is rewired across scales, correlated with gene expression modules, and independent of sensory experience. Finally, I examined allele-specific structure of imprinted genes, revealing local and chromosome-wide differences. More recently, I expanded my 3D genome atlas to the human and mouse cerebellum—the most consistently affected brain region in autism. I uncovered unique 3D genome rewiring throughout life, providing a structural basis for the cerebellum’s unique mode of development and aging. In addition, to accurately measure de novo mutations in a single cell, I developed a new method—multiplex end-tagging amplification of complementary strands (META-CS), which eliminates nearly all false positives by virtue of DNA complementarity. Using META-CS, I determined the true mutation spectrum of single human brain cells, free from chemical artifacts. Together, my findings uncovered an unknown dimension of neurodevelopment, and open up opportunities for new treatments for autism and other developmental disorders.

Brain oxytocin as a modulator of social approach versus avoidance

Brain dynamics and flexible behaviors

Executive control processes and flexible behaviors rely on the integrity of, and dynamic interactions between, large-scale functional brain networks. The right insular cortex is a critical component of a salience/midcingulo-insular network that is thought to mediate interactions between brain networks involved in externally oriented (central executive/lateral frontoparietal network) and internally oriented (default mode/medial frontoparietal network) processes. How these brain systems reconfigure with development is a critical question for cognitive neuroscience, with implications for neurodevelopmental pathologies affecting brain connectivity. I will describe studies examining how brain network dynamics support flexible behaviors in typical and atypical development, presenting evidence suggesting a unique role for the dorsal anterior insular from studies of meta-analytic connectivity modeling, dynamic functional connectivity, and structural connectivity. These findings from adults, typically developing children, and children with autism suggest that structural and functional maturation of insular pathways is a critical component of the process by which human brain networks mature to support complex, flexible cognitive processes throughout the lifespan.

One by one: brain organoid modelling of neurodevelopmental disorders at single cell resolution

Studying cortical development through the lens of autism spectrum disorders

SELECTIVE ATTENTION AND EXECUTIVE CONTROL IN AUTISM SPECTRUM DISORDER AND SCHIZOPHRENIA: AN EYE MOVEMENT STUDY

FENS Forum 2026

LATENT STRUCTURE AND BEHAVIOURAL HETEROGENEITY OF RESTRICTED AND REPETITIVE BEHAVIOURS IN AUTISM USING ORDINAL ADI-R DATA

FENS Forum 2026

THALAMOCORTICAL ENCODING OF TACTILE STIMULI IN THE <EM>SHANK3 </EM>KO MOUSE MODEL OF AUTISM SPECTRUM DISORDER

FENS Forum 2026

CARDIAC INTEROCEPTION AND INSULAR CORTEX: A PATHWAY TO UNDERSTANDING SOCIAL DEFICITS IN AUTISM

FENS Forum 2026

USING THE MICECRAFT SYSTEM TO STUDY SOCIAL MOTIVATION, COGNITION AND NEURONAL ACTIVITY IN AUTISM MOUSE MODELS

FENS Forum 2026

RETROSPLENIAL CORTEX INVOLVEMENT IN NOVELTY EXPLORATION ALTERATIONS IN A MOUSE MODEL OF AUTISM

FENS Forum 2026

LOCALIZED STRUCTURAL HYPER-CONNECTIVITY IN ADULT AUTISM: EVIDENCE FROM MORPHOMETRIC INVERSE DIVERGENCE

FENS Forum 2026

DOPAMINE DYNAMICS REGULATE SOCIAL INTERACTION IN A VALPROIC ACID MODEL OF AUTISM

FENS Forum 2026

EARLY ONSET OF CEREBELLAR AND PERIPHERAL INFLAMMATION IN CNTNAP2 AND SHANK3B MOUSE MODELS OF AUTISM

FENS Forum 2026

THE NEUROLIGIN-3 R451C VARIANT IMPACTS INFLAMMATORY RESPONSES: SEX-SPECIFIC RESILIENCE FOLLOWING DSS-INDUCED COLITIS IN A MOUSE MODEL OF AUTISM

FENS Forum 2026

NARP-RELATED ALTERATIONS IN THE EXCITATORY AND INHIBITORY CIRCUITRY OF SOCIALLY ISOLATED MICE: DEVELOPMENTAL INSIGHTS AND IMPLICATIONS FOR AUTISM SPECTRUM DISORDER

FENS Forum 2026

THE AUTISM RISK GENE <EM>CNTN4</EM> REGULATES AMPA RECEPTOR EXPRESSION IN NEURONS

FENS Forum 2026

COMPARATIVE MOLECULAR CONNECTOMICS TO UNCOVER THE IMPACT OF MUTATIONS IN AUTISM RISK GENES<EM > IN VIVO</EM>

FENS Forum 2026

RETROSPLENIAL CORTEX INVOLVEMENT IN NOVELTY EXPLORATION ALTERATIONS IN A MOUSE MODEL OF AUTISM

FENS Forum 2026

A NOVEL PHENOTYPE BATTERY FOR ENHANCING GENETIC DIAGNOSIS OF AUTISM SPECTRUM DISORDER

FENS Forum 2026

ST-2657, A DUAL G9A/H3R MODULATOR, AMELIORATES BEHAVIORAL DEFICITS, OXIDATIVE STRESS AND NEUROINFLAMMATION AND RESTORES NEUROPLASTICITY IN BTBR MICE MODEL OF AUTISM

FENS Forum 2026

SPOT THE DIFFERENCE: WHOLE-BRAIN CLEARING AND MULTICHANNEL IMAGING TO MAP SEX-DEPENDENT BRAIN CELL DIFFERENCES IN MOUSE MODELS OF AUTISM SPECTRUM DISORDER

FENS Forum 2026

EXPOSURE TO THE ANTIOXIDANT FOLIUM ALLEVIATES OXIDATIVE STRESS IN A VALPROIC ACID-INDUCED ANIMAL MODEL OF AUTISM

FENS Forum 2026

MOLECULAR MECHANISM UNDERLYING BRAIN ASYMMETRY AND AUTISM

FENS Forum 2026

MECHANISMS OF MOTOR IMPAIRMENTS IN AUTISM SPECTRUM DISORDER

FENS Forum 2026

PERIPHERAL NEUROIMMUNE MECHANISMS UNDERLYING MECHANICAL ITCH HYPERSENSITIVITY ASSOCIATED WITH AUTISM SPECTRUM DISORDERS

FENS Forum 2026

IDENTIFYING RELATIONSHIPS BETWEEN LATENT SUBTYPES OF SOCIAL BEHAVIOUR AND SNP VARIATION IN AUTISM SPECTRUM DISORDER

FENS Forum 2026

RESTORING THE CLOCK: CIRCADIAN RHYTHM MODULATION AS A NOVEL THERAPY FOR SCN2A-ASSOCIATED AUTISM SPECTRUM DISORDER

FENS Forum 2026

CHARACTERIZATION OF AUTISM-ASSOCIATED <EM>DLGAP2/FBXO25 </EM>DOUBLE MUTANT MICE

FENS Forum 2026

A NEW MOUSE MODEL OF NON-SYNDROMIC AUTISM SPECTRUM DISORDER CARRYING THE HUMAN NEGATIVE-DOMINANT MUTATION L1314P OF THE<EM> SCN2A/</EM>NA<SUB>V</SUB>1.2 SODIUM CHANNEL

FENS Forum 2026

SELENOPROTEIN T MIMETIC, PSELT, AMELIORATES BEHAVIORAL ALTERATIONS AND OXIDATIVE STRESS IN A PRENATAL VALPROIC ACID MOUSE MODEL OF AUTISM

FENS Forum 2026

DIFFERENTIAL GENOTYPE-PHENOTYPE CORRELATION ACROSS SOCIAL AND SENSORY DOMAINS IN THE HETEROZYGOUS SHANK3B MOUSE MODEL OF AUTISM SPECTRUM DISORDER

FENS Forum 2026

OXYTOCIN MODULATES SOCIAL SALIENCE NETWORK CONNECTIVITY IN AUTISM

FENS Forum 2026

PAX5 DEFICIENCY DISRUPTS MIDBRAIN GABAERGIC DEVELOPMENT IN A MOUSE MODEL OF AUTISM SPECTRUM DISORDER

FENS Forum 2026

MGLU4-TARGETING NANOBODIES RESTORE SOCIAL BEHAVIOR IN MOUSE MODELS OF AUTISM SPECTRUM DISORDERS

FENS Forum 2026

5-HT7 RECEPTOR UPREGULATION AND LP-211 TREATMENT REVERSE ELECTROPHYSIOLOGICAL AND BEHAVIORAL DEFICITS IN A VALPROIC ACID–INDUCED RAT MODEL OF AUTISM

FENS Forum 2026

​ALTERATIONS IN PREFRONTAL CORTEX FUNCTION IN THE <EM>​FMR1</EM>KO MOUSE MODEL OF AUTISM AND FRAGILE X SYNDROME

FENS Forum 2026

ALTERED NOCICEPTIVE RESPONDING IN A PRECLINICAL MODEL OF AUTISM IS ASSOCIATED WITH SEX-DEPENDANT TRANSCRIPTIONAL CHANGES IN THE DORSAL HORN OF THE SPINAL CORD

FENS Forum 2026

THE ROLE OF THE MEDIAL PREFRONTAL CORTEX IN TEMPORAL MULTISENSORY INTEGRATION DEFICITS IN MOUSE MODELS OF AUTISM

FENS Forum 2026

VALPROIC ACID RAT MODELS OF AUTISM SPECTRUM DISORDER SHOW NO BEHAVIORAL FLEXIBILITY DEFICITS IN A VARIABLE INTERVAL REVERSAL LEARNING TASK

FENS Forum 2026

A CELL-TYPE SPECIFIC MUTATION OF THE AUTISM CANDIDATE GENE REELIN IN SOMATOSTATIN CORTICAL NEURONS RESULTS IN SELECTIVE AUTISTIC-LIKE BEHAVIOURAL ALTERATIONS IN MICE

FENS Forum 2026

AUDITORY ENTRAINMENT REVERSES WORKING MEMORY DEFICITS IN A RODENT MODEL OF AUTISM

FENS Forum 2026

THE SYNAPTIC ROLE OF CADHERIN-13, A PROTEIN ASSOCIATED WITH AUTISM SPECTRUM DISORDERS (ASD)

FENS Forum 2026

LINK BETWEEN HCN CHANNELOPATHY AND AUDITORY HYPERSENSITIVITY IN A MOUSE MODEL OF AUTISM SPECTRUM DISORDER

FENS Forum 2026

VITAMIN A STATUS MODULATES NEURODEVELOPMENTAL, OXIDATIVE, AND CHOLINERGIC ALTERATIONS IN A VALPROIC ACID–INDUCED RAT MODEL OF AUTISM

FENS Forum 2026