Autism Spectrum Disorder
autism spectrum disorder
Georgia Panagiotakos
Looking for a supportive, dynamic and inclusive environment to do cutting edge science? The Panagiotakos Lab at Mount Sinai has two postdoctoral positions open! Links for both positions below – come join us if you love neural development, ion channels or anything in between! The Panagiotakos Lab, in the Departments of Psychiatry and Neuroscience at the Icahn School of Medicine at Mount Sinai in New York, is seeking postdoctoral fellows (recently completed Ph.D., M.D. or M.D./Ph.D.) with expertise in calcium imaging, electrophysiology, developmental neuroscience, stem cell biology, and/or genomics/sequencing approaches to study cellular and molecular mechanisms that underlie the acquisition of cell fate during mammalian brain development. Dr. Panagiotakos’ team combines multiple complementary approaches, including genetic mouse models, calcium imaging, fluorescence microscopy, pharmacology, cortical slice cultures, and various omics and biochemical analyses, to interrogate roles for calcium signaling, electrical activity, ion channel splice isoforms, and disease risk genes during normal development and in the context of neuropsychiatric disorders of developmental origin. The qualified candidates will use cutting-edge cellular/molecular biology, imaging and sequencing approaches in these studies, including long-isoform sequencing, CUT&RUN, and live imaging, to investigate the impact and mechanistic underpinnings of disease-relevant ion channels and calcium signaling on cellular events during brain development, including proliferation, migration, neurogenesis and gliogenesis.
Dr. Amir Aly
We are pleased to announce an opportunity for a tax-free fully funded PhD studentship - Multimodal AI-based Diagnosis of Attention Deficit Hyperactivity Disorder (ADHD) - at Plymouth University, UK. This exciting project aims to transform ADHD diagnosis by developing a multimodal Artificial Intelligence (AI) framework that addresses the significant limitations of current, subjective diagnostic practices. Although AI is emerging in ADHD research, its integration into standard clinical practices remains minimal. This project seeks to enhance diagnostic accuracy through a sophisticated integration of AI-driven insights that complement existing approaches. Some basic questions (among others) that this project will try to explore are: How can machine learning and deep learning models be tailored to various data types like neuroimaging to uncover distinct ADHD diagnostic patterns? What methods can be used to analyse fMRI data to delineate active brain regions and their connections, and how can these findings be linked to ADHD behaviours and cognitive functions? How can we refine AI models to handle high data dimensionality and heterogeneity and enhance decision-making transparency in clinical settings using Explainable AI (XAI) methods? What are the best practices to assess the robustness of AI models against the variability in ADHD diagnostic data? This ambitious project will allow the student to engage in a groundbreaking study at the intersection of AI, neuropsychiatry, and healthcare and gain experience in a highly collaborative environment supported by a strong supervisory team and international experts. The research leverages our team's extensive background in neuro-developmental disorders like Autism Spectrum Disorder (ASD), where we recently discussed important brain regions related to ASD diagnosis. This PhD opportunity offers a deep dive not only into the diagnosis of ADHD using explainable AI but also into other related co-occurring disorders like ASD, providing a holistic perspective on patient care and intervention strategies across the spectrum of these interrelated conditions.
Dr. Amir Aly
We are pleased to announce an opportunity for a tax-free fully funded PhD studentship - Multimodal AI-based Diagnosis of Attention Deficit Hyperactivity Disorder (ADHD) - at Plymouth University, UK. This exciting project aims to transform ADHD diagnosis by developing a multimodal Artificial Intelligence (AI) framework that addresses the significant limitations of current, subjective diagnostic practices. Although AI is emerging in ADHD research, its integration into standard clinical practices remains minimal. This project seeks to enhance diagnostic accuracy through a sophisticated integration of AI-driven insights that complement existing approaches. Some basic questions (among others) that this project will try to explore are: How can machine learning and deep learning models be tailored to various data types like neuroimaging to uncover distinct ADHD diagnostic patterns? What methods can be used to analyse fMRI data to delineate active brain regions and their connections, and how can these findings be linked to ADHD behaviours and cognitive functions? How can we refine AI models to handle high data dimensionality and heterogeneity and enhance decision-making transparency in clinical settings using Explainable AI (XAI) methods? What are the best practices to assess the robustness of AI models against the variability in ADHD diagnostic data? This ambitious project will allow the student to engage in a groundbreaking study at the intersection of AI, neuropsychiatry, and healthcare and gain experience in a highly collaborative environment supported by a strong supervisory team and international experts. The research leverages our team's extensive background in neuro-developmental disorders like Autism Spectrum Disorder (ASD), where we recently discussed important brain regions related to ASD diagnosis. This PhD opportunity offers a deep dive not only into the diagnosis of ADHD using explainable AI but also into other related co-occurring disorders like ASD, providing a holistic perspective on patient care and intervention strategies across the spectrum of these interrelated conditions.
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.
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.
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.
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.
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
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
Studying cortical development through the lens of autism spectrum disorders
Keeping your Brain in Balance: the Ups and Downs of Homeostatic Plasticity (virtual)
Our brains must generate and maintain stable activity patterns over decades of life, despite the dramatic changes in circuit connectivity and function induced by learning and experience-dependent plasticity. How do our brains acheive this balance between opposing need for plasticity and stability? Over the past two decades, we and others have uncovered a family of “homeostatic” negative feedback mechanisms that are theorized to stabilize overall brain activity while allowing specific connections to be reconfigured by experience. Here I discuss recent work in which we demonstrate that individual neocortical neurons in freely behaving animals indeed have a homeostatic activity set-point, to which they return in the face of perturbations. Intriguingly, this firing rate homeostasis is gated by sleep/wake states in a manner that depends on the direction of homeostatic regulation: upward-firing rate homeostasis occurs selectively during periods of active wake, while downward-firing rate homeostasis occurs selectively during periods of sleep, suggesting that an important function of sleep is to temporally segregate bidirectional plasticity. Finally, we show that firing rate homeostasis is compromised in an animal model of autism spectrum disorder. Together our findings suggest that loss of homeostatic plasticity in some neurological disorders may render central circuits unable to compensate for the normal perturbations induced by development and learning.
Reward system function and dysfunction in Autism Spectrum Disorders
Gut-brain signaling as a driver of behavior and gene expression in a mouse model for autism spectrum disorder
Gestational exposure to environmental toxins, infections, and stressors are epidemiologically linked to neurodevelopmental disorders
Gestational exposure to environmental toxins, infections, and stressors are epidemiologically linked to neurodevelopmental disorders with strong male-bias, such as autism spectrum disorder. We modeled some of these prenatal risk factors in mice, by co-exposing pregnant dams to an environmental pollutant and limited-resource stress, which robustly dysregulated the maternal immune system. Male but not female offspring displayed long-lasting behavioral abnormalities and alterations in the activity of brain networks encoding social interactions, along with disruptions of gut structure and microbiome composition. Cellularly, prenatal stressors impaired microglial synaptic pruning in males during early postnatal development. Precise inhibition of microglial phagocytosis during the same critical period mimicked the impact of prenatal stressors on the male-specific social deficits. Conversely, modifying the gut microbiome rescued the social and cellular deficits, indicating that environmental stressors alter neural circuit formation in males via impairing microglia function during development, perhaps via a gut-brain disruption.
Making memories in mice
Understanding how the brain uses information is a fundamental goal of neuroscience. Several human disorders (ranging from autism spectrum disorder to PTSD to Alzheimer’s disease) may stem from disrupted information processing. Therefore, this basic knowledge is not only critical for understanding normal brain function, but also vital for the development of new treatment strategies for these disorders. Memory may be defined as the retention over time of internal representations gained through experience, and the capacity to reconstruct these representations at later times. Long-lasting physical brain changes (‘engrams’) are thought to encode these internal representations. The concept of a physical memory trace likely originated in ancient Greece, although it wasn’t until 1904 that Richard Semon first coined the term ‘engram’. Despite its long history, finding a specific engram has been challenging, likely because an engram is encoded at multiple levels (epigenetic, synaptic, cell assembly). My lab is interested in understanding how specific neurons are recruited or allocated to an engram, and how neuronal membership in an engram may change over time or with new experience. Here I will describe both older and new unpublished data in our efforts to understand memories in mice.
miRNA dysregulation in embryo results in autism spectrum disorder
Investigating the environmental etiology of autism spectrum disorder
Circuit homeostasis: keeping a level head when the brain gets hot
Core body temperature is regulated to a setpoint between 36.1 to 37.8°C, with an average fluctuation of 0.5°C during a 24-hour day. Despite mechanistic safeguards, major temperature deviations (1-3°C) from the setpoint occur in the body and in turn the brain. For unknown reasons, in most mammals (humans included), these increases in brain temperature are benign. However, macro-fluctuations in brain temperature in some cases result in deleterious outcomes such as seizures. In this talk, I will describe a mechanism for circuit-level adaptive regulation of cortical activity during macro-fluctuations in brain temperature. I will also discuss how this mechanism can be applied towards the understanding of the pathology of Autism Spectrum Disorder.
New Strategies and Approaches to Tackle and Understand Neurological Disorder
Broadly, the Mauro Costa-Mattioli laboratory (The MCM Lab) encompasses two complementary lines of research. The first one, more traditional but very important, aims at unraveling the molecular mechanisms underlying memory formation (e.g., using state-of-the-art molecular and cell-specific genetic approaches). Learning and memory disorders can strike the brain during development (e.g., Autism Spectrum Disorders and Down Syndrome), as well as during adulthood (e.g., Alzheimer’s disease). We are interested in understanding the specific circuits and molecular pathways that are primarily targeted in these disorders and how they can be restored. To tackle these questions, we use a multidisciplinary, convergent and cross-species approach that combines mouse and fly genetics, molecular biology, electrophysiology, stem cell biology, optogenetics and behavioral techniques. The second line of research, more recent and relatively unexplored, is focused on understanding how gut microbes control CNS driven-behavior and brain function. Our recent discoveries, that microbes in the gut could modulate brain function and behavior in a very powerful way, have added a whole new dimension to the classic view of how complex behaviors are controlled. The unexpected findings have opened new avenues of study for us and are currently driving my lab to answer a host of new and very interesting questions: - What are the gut microbes (and metabolites) that regulate CNS-driven behaviors? Would it be possible to develop an unbiased screening method to identify specific microbes that regulate different behaviors? - If this is the case, can we identify how members of the gut microbiome (and their metabolites) mechanistically influence brain function? - What is the communication channel between the gut microbiota and the brain? Do different gut microbes use different ways to interact with the brain? - Could disruption of the gut microbial ecology cause neurodevelopmental dysfunction? If so, what is the impact of disruption in young and adult animals? - More importantly, could specific restoration of selected bacterial strains (new generation probiotics) represent a novel therapeutic approach for the targeted treatment of neurodevelopmental disorders? - Finally, can we develop microbiota-directed therapeutic foods to repair brain dysfunction in a variety of neurological disorders?
Promises and pitfalls in going from the bench to the bedside in autism spectrum disorder
Understanding the cellular and molecular landscape of autism spectrum disorders
Large genomic studies of individuals with autism spectrum disorders (ASD) have revealed approximately 100-200 high risk genes. However, whether these genes function in similar or different signaling networks in brain cells (neurons) remains poorly studied. We are using proteomic technology to build an ASD-associated signaling network map as a resource for the Autism research community. This resource can be used to study Autism risk genes and understand how pathways are convergent, and how patient mutations change the interaction profile. In this presentation, we will present how we developed a pipeline using neurons to build protein-protein interaction profiles. We detected previously unknown interactions between different ASD risk genes that have never been linked together before, and for some genes, we identified new signaling pathways that have not been previously reported. This resource will be available to the research community and will foster collaborations between ASD researchers to help accelerate therapeutics for ASD and related disorders.
Molecular Biology of the Fragile X Syndrome
Silencing of FMR1 and loss of its gene product, FMRP, results in fragile X syndrome (FXS). FMRP binds brain mRNAs and inhibits polypeptide elongation. Using ribosome profiling of the hippocampus, we find that ribosome footprint levels in Fmr1-deficient tissue mostly reflect changes in RNA abundance. Profiling over a time course of ribosome runoff in wild-type tissue reveals a wide range of ribosome translocation rates; on many mRNAs, the ribosomes are stalled. Sucrose gradient ultracentrifugation of hippocampal slices after ribosome runoff reveals that FMRP co-sediments with stalled ribosomes, and its loss results in decline of ribosome stalling on specific mRNAs. One such mRNA encodes SETD2, a lysine methyltransferase that catalyzes H3K36me3. Chromatin immunoprecipitation sequencing (ChIP-seq) demonstrates that loss of FMRP alters the deployment of this histone mark. H3K36me3 is associated with alternative pre-RNA processing, which we find occurs in an FMRP-dependent manner on transcripts linked to neural function and autism spectrum disorders.
Towards therapeutics for Autism Spectrum Disorder using Syngap1 heterozygous mouse model
Autism-Associated Shank3 Is Essential for Homeostatic Compensation in Rodent Visual Cortex
Neocortical networks must generate and maintain stable activity patterns despite perturbations induced by learning and experience- dependent plasticity. There is abundant theoretical and experimental evidence that network stability is achieved through homeostatic plasticity mechanisms that adjust synaptic and neuronal properties to stabilize some measure of average activity, and this process has been extensively studied in primary visual cortex (V1), where chronic visual deprivation induces an initial drop in activity and ensemble average firing rates (FRs), but over time activity is restored to baseline despite continued deprivation. Here I discuss recent work from the lab in which we followed this FR homeostasis in individual V1 neurons in freely behaving animals during a prolonged visual deprivation/eye-reopening paradigm. We find that - when FRs are perturbed by manipulating sensory experience - over time they return precisely to a cell-autonomous set-point. Finally, we find that homeostatic plasticity is perturbed in a mouse model of Autism spectrum disorder, and this results in a breakdown of FRH within V1. These data suggest that loss of homeostatic plasticity is one primary cause of excitation/inhibition imbalances in ASD models. Together these studies illuminate the role of stabilizing plasticity mechanisms in the ability of neocortical circuits to recover robust function following challenges to their excitability.
Autism spectrum disorder: from gene discovery to functional insights
Autism spectrum disorder (ASD) is a neurodevelopmental disorder affecting up to 1% of the population. Over the past few years, large-scale genomic studies have identified hundreds of genetic loci associated with liability to ASD. It is now time to translate these genetic discoveries into functional studies that can help us understand convergences and divergences across risk genes, and build pre-clinical cell and animal models. In this seminar, I will discuss some of the most recent findings on the genetic risk architecture of ASD. I will then expand on our work on biomarkers discovery and neurodevelopmental analyses in two rare genetic conditions associated with ASD: ADNP and DDX3X syndrome.
Machine learning of functional network and molecular mechanisms in autism spectrum disorder subtypes
COSYNE 2023
The anti-reward center in Autism Spectrum Disorders (ASDs)
FENS Forum 2024
Brain activation patterns in patients with autism spectrum disorder in pain-related perspective-taking: Relationship with interoceptive accuracy
FENS Forum 2024
Changes in striatal spiny projection neurons’ properties and circuitry in a mouse model of autism spectrum disorder with cholinergic interneuron dysfunction
FENS Forum 2024
Characterization of the transcriptional landscape of endogenous retroviruses at the fetal-maternal interface in a mouse model of autism spectrum disorder
FENS Forum 2024
Characterizing age-related cognitive-motor interactions in individuals with and without autism spectrum disorder using mobile brain-body imaging (MoBI)
FENS Forum 2024
Deciphering the neurodevelopmental role of the brain secretome in Autism Spectrum Disorder
FENS Forum 2024
Effect of ENERGI in valproate-induced animal with autism spectrum disorder
FENS Forum 2024
Electrophysiologic, transcriptomic, and morphologic plasticity of spinal inhibitory neurons to decipher atypical mechanosensory perception in Autism Spectrum Disorder
FENS Forum 2024
Exploring altered translation in autism spectrum disorder
FENS Forum 2024
GPR50-mediated mitophagy in the pathogenesis of autism spectrum disorders
FENS Forum 2024
Hyposensitivity to thermal stimulus with prefrontal cortical implication in two animal models of autism spectrum disorder
FENS Forum 2024
The impact of autism spectrum disorder-risk genes on human neural stem cell proliferation and survival
FENS Forum 2024
Impact of a cocktail of fungicides at the regulatory dose in Europe on the neurodevelopment of a mice model of Autism Spectrum Disorders (ASD)
FENS Forum 2024
Impaired excitatory and inhibitory synaptic plasticity in the NLGN3-R451C mouse model of autism spectrum disorder
FENS Forum 2024
Investigating the role of the PTCHD1-PTCHD1-AS risk locus in Autism Spectrum Disorder
FENS Forum 2024
Involvement of amygdala neurons in male predominance of Autism Spectrum Disorder
FENS Forum 2024
Mapping the cell state landscape of autism spectrum disorders
FENS Forum 2024
The mGlu4 positive allosteric modulator foliglurax durably rescues behavioral deficits in three mouse models of autism spectrum disorder
FENS Forum 2024
mTOR pathway disruption in GABAergic neurons impacts morphological and functional development of cortical and thalamic somatosensory areas in a mouse model of autism spectrum disorder
FENS Forum 2024
Neuronal activities during a VR-based assessment for Autism Spectrum Disorder: A pilot EEG study
FENS Forum 2024
Neuronal correlates of increased behavioral inhibition by interoceptive stimulation in a mouse model of autism spectrum disorder
FENS Forum 2024
Neurophysiology of perceptual closure abilities in children with autism spectrum disorder and neurotypical control children
FENS Forum 2024
De novo variants in SP9 cause a novel form of interneuronopathy characterized by intellectual disability, autism spectrum disorder, and epilepsy with variable expressivity
FENS Forum 2024
Olfactory discrimination and reversal learning in the Neurexin1 (+/-) mouse model of autism spectrum disorder
FENS Forum 2024
Oxytocin ameliorates aggression in a mouse model of autism spectrum disorder (ASD)
FENS Forum 2024
Prefrontal cortex alterations underlying attentional modulation of sensory information in the Fmr1KO mouse model of autism spectrum disorder
FENS Forum 2024
Rectifying interneuron developmental trajectory prevents the core symptoms of autism spectrum disorder in mice
FENS Forum 2024
The selective deletion of an autism spectrum disorder associated gene in a neuronal subpopulation causes subtle anxiety-related abnormalities
FENS Forum 2024
The social behaviorome in mouse models of autism spectrum disorders (ASD)
FENS Forum 2024
Tactile sensory processing deficits in the Shank3 KO mouse model of autism spectrum disorder
FENS Forum 2024
Unraveling gender disparities in autism spectrum disorders: The impact of immunological factors in a mouse model of autism
FENS Forum 2024
Upregulation of Negr1 converges into core impaired processes in autism spectrum disorders
FENS Forum 2024