ASN 2026

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ASN 2026 Detailed Program

Below is the final detailed program information for the ASN 2026 Annual Meeting.

 

Astrocyte Regulation of Neuronal Function in Health and Disease: From Synapses to Behavior
Dr. Elena Blanco-Suarez
Astrocytes and other non-neuronal brain cells play a central, yet often underappreciated, role in shaping neuronal function. While it is clear that neuron–glia interactions are essential for brain development, plasticity, and behavior, the molecular and cellular mechanisms by which astrocytes influence neurons remain an exciting frontier. This symposium will showcase cutting-edge research uncovering how astrocytes regulate neuronal communication and behavior across both healthy and diseased brain states, offering fresh insights into the complex cellular choreography that underlies behavior and synaptic health.
Additional sessions should follow this same format.

Astrocytes have emerged as key neural hubs controlling circuit dynamics and behavior in the past decade. Combining in-vivo recordings of astrocyte calcium activity, GRAB sensors technologies, multi-omics, physiology, behavioral tracking and computational modeling, recent advances are shining light on the real-time interplay between astrocyte signaling and neuromodulator dynamics during behavior, and how they are influenced by context. This symposium will highlight cutting-edge research from rising stars and established leaders in the field whose work is at the forefront of global efforts to uncover how astrocytes encode behavioral parameters and contribute to circuit operations that underly observable behavior.

Focus in theoretical and computational neuroscience has traditionally been directed at neurons and synaptic connectivity as the primary mediators of information processing in the brain. This view is beginning to be reshaped by a recognition of multicellular contributions to neural computation, including by astrocytes. Astrocytes actively influence synaptic transmission, neuronal excitability, and blood flow, suggesting they play not just a supportive role, but may be pivot points in the propagation or gating of functionally salient signals throughout the brain. Indeed, the molecular diversity of astrocytes and their spatiotemporally hierarchical interactions with neurons makes them potentially uniquely suited to significantly impact plasticity and other key aspects of learning and information processing. This session will explore how computational modeling is being used to explore how astrocytes enhance neural circuit dynamics and function. Through this computational lens, the invited talks will present new models and theories regarding neural-astrocyte interaction and brain function.

Astrocytes have long been assumed to play a central role in the formation, maintenance, and repair of the blood-brain barrier (BBB). These assumptions stem from early co-culture and transplantation studies, as well as the close anatomical relationship between astrocyte endfeet and the vasculature. More recent findings, however, have challenged the extent of astrocyte influence—highlighting pericytes and even neurons as key regulators of barrier integrity, particularly during development.

This symposium invites a critical reexamination of BBB biology. A central challenge is to understand how cellular and molecular mechanisms of BBB regulation differ across developmental, adult, and disease contexts. Do the same pathways that guide BBB formation also support its maintenance in the adult brain or promote repair after injury? Are distinct molecular programs activated in response to stress or cell-type interactions? These questions are increasingly urgent, as BBB dysfunction is now recognized as an early driver of neurodegenerative diseases.

The session will explore how CNS cell types—including astrocytes, pericytes, and neurons–regulate the BBB in diverse experimental systems. Talks will highlight neuron-derived signals in BBB formation, astrocyte-mediated support of adult BBB maintenance and interference with repair, the role of Connexin43 and gap junctions in BBB integrity in neurovascular disease, and how pericyte vulnerability contributes to dysfunction in HIV and stroke. Collectively, these presentations will illuminate the dynamic, context-specific roles of CNS cells in shaping BBB function.

This proposal aligns with ASN’s themes in Glial Cell Biology, Building the Nervous System, Cell & Molecular Neurobiology, and Neurodegeneration.

Dopamine has long been recognized as a critical regulator of brain function, psychostimulant action, and reward processes. However, emerging research reveals that, in addition to its central function, dopamine is a dynamic regulator of the intersystemic interactions between brain and body. This symposium will explore the expanding functional repertoire of dopamine, including how changes in dopamine function influence peripheral systems and how peripheral signals, in turn, regulate central dopamine dynamics. The symposium will feature recent mechanistic insights into how changes in the activity of dopamine neurons regulates peripheral immunity and spleen phenotype, how hormones traditionally known for their roles in feeding, can regulate central dopamine function, leading to reduced responses to cocaine, revealing novel avenues for therapeutic interventions. Additional presentations will examine how dopamine regulates peripheral immune cells function, gut-brain communication, and neuroinflammatory responses, highlighting dopamine’s role in bi-directional neurochemical signaling. Finally, new mechanistic insights into how changes in microbiome composition regulates dopamine neurotransmission will also be discussed. Collectively, the session will provide an integrative perspective on dopamine as signaling hub, incorporating molecular pharmacology, behavioral neuroscience, and systems neurobiology. By illuminating the crosstalk between dopamine signaling and peripheral physiology, we aim to reframe dopamine within the broader context of brain-body homeostasis.

Effective pharmacological treatment of neurological disorders is challenged by the cellular diversity and inaccessibility of the nervous system, often leading to prolonged dysfunction because of ineffective delivery of appropriate concentrations of therapeutics. This has prompted the development of several species of new therapeutic delivery systems that take advantage of the unique attributes of materials at the nanoscale that differ from their bulk characteristics, leading to the creation of nanomaterial systems that are well-tolerated, can deliver effective therapeutic doses to specific sites or cells, allow for on-demand release of the therapeutics, and can readily cross biological barriers. In this session, three accomplished neuroscientists at different career levels will provide updates on nanoscale systems designed to treat several types of neurological disorders. Topics will include axon regeneration, peripheral neuropathy, brain tumors, stroke, and spinal cord injury. Specific topics to be discussed are drug delivery across the blood nerve barrier to treat peripheral neuropathy, use of nanomaterials to deliver therapeutics across the blood brain barrier, and nanomaterial targeting of corticospinal tract neurons to encourage recovery of motor function.

Abnormal expansion of short DNA repeat sequences within specific genes causes several devastating neurodegenerative diseases. Among the most notable are the GGGGCC repeat expansion in C9orf72, the most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia (C9ALS/FTD), and expanded CAG repeats in the HTT gene, which cause Huntington’s disease (HD). These disorders share overlapping pathogenic mechanisms, including toxic RNA and protein accumulation, RAN translation, polyglutamine expansion, disrupted RNA metabolism, nucleocytoplasmic transport defects, and dysfunction in both neurons and glia.

This symposium will present new insights into disease mechanisms and the development of therapeutic approaches. Zhu will discuss how gain-of-toxicity and loss-of-function mechanisms converge in C9ALS/FTD through distinct effects on neurons and glia, and the therapeutic strategies needed to address both. Gao will highlight discoveries from Drosophila and iPSC models and their applications in therapeutic development. Sattler will present recent findings on RNA editing and its role in regulating TDP-43 nuclear export. Duan will discuss glymphatic system dysfunction and potential therapeutic approaches in HD. Bogdan will showcase the application of Multimodal MERFISH in HD—an advanced spatial transcriptomics platform enabling single-cell transcriptomic profiling alongside quantification of huntingtin aggregates and somatic CAG repeat expansions.

This session will integrate molecular, cellular, and translational perspectives, and feature emerging therapeutic strategies such as ASOs, gene expression modulation, and spatial genomics tools. The symposium will provide a valuable forum to explore diverse aspects of repeat expansion-mediated neurodegeneration and discuss future directions.

Post-translational modifications (PTMs) are crucial protein folding, function, and localization regulators. Dysregulation of PTMs increasingly emerges as a driving factor in neurological and neurodegenerative diseases. Among these, citrullination, catalyzed by peptidylarginine deiminases, plays a significant role in neurodegeneration, with notable impact in conditions such as multiple sclerosis and frontotemporal dementia. Concurrently, lysine acetylation, historically studied in nuclear and cytosolic compartments, has been recently identified in the endoplasmic reticulum (ER), revealing novel layers of intracellular signaling and protein quality control. This process is governed by the ER-acetylation machinery, including the cytosol-to-ER-lumen acetyl-CoA transporter AT-1. Dysfunctional ER-based acetylation, caused by overexpression of the acetyl-CoA transporter AT-1, results in altered glycoprotein flux through the secretory pathway and an autistic-like phenotype. Arginylation modulates cytoskeletal dynamics, protein turnover, and stress responses, and has been implicated in brain aging and neurodegeneration. The ‘cross-talk’ between arginylation, citrullination, and acetylation in neuronal and glial contexts has significant downstream effects, such as influencing the recruitment of specific ‘reader’ proteins, further impacting protein folding, protein-protein interactions, and biological processes like gene expression. This symposium session will focus on the pathological relevance and mechanistic interplay of these PTMs in neuronal and glial contexts. Key topics include citrullination in glial cells and myelin disorders, the intracellular citrate/acetyl-CoA flux, and ER-acetylation machinery in neurodevelopmental disorders, arginylation as a novel biological regulator of brain proteins, and PTM-driven modulation of RNA-binding proteins such as TDP-43 in neurodegenerative disorders. These insights will highlight how PTM interplay reshapes neurobiology across cellular systems and disease states.

In this session, we will present four distinct approaches to leveraging glial biology to improve CNS repair, with a particular focus on repair in models of dementia. By highlighting multiple glial populations and intervention strategies, we will showcase the breadth of promising glial research in this area of high unmet clinical need.

Stem cell–based strategies are rapidly transforming the landscape of CNS repair, offering new ways to restore function in a range of neurological diseases. Dr. Irene L. Llorente will present advances in human iPSC-derived glial progenitors as a novel therapeutic platform, highlighting their rapid production, stable lineage commitment, and targeted efficacy in white matter repair across models of stroke and neurodegeneration.

Cerebrovascular dysfunction is one of the earliest symptoms of multiple forms of dementia, and is largely regulated by pericytes. Dr. Andy Shih will discuss the promise of manipulating pericytes to improve cerebrovascular health, particularly in Alzheimer’s disease.

The innate immune system, including microglia, is increasingly recognized to play critical roles in numerous neurologic diseases. Dr. John Lukens will discuss the roles of this multicellular system in neurodegenerative disease.

Astrocytes respond dramatically to brain perturbations; this reactivity is calibrated to the particular insult and can be brain region-dependent. Dr. Amy Gleichman will present examples of reactive astrocyte heterogeneity and how these differential responses can inform new strategies to promote brain repair.

Lipids make up approximately 50% of the brain’s dry weight. Lipids are not just passive structural components but active players in the intricate neurochemistry of the brain. Alterations in brain lipid homeostasis are increasingly recognized as contributing factors to the etiology and progression of various neurological cancers and neurodegenerative diseases. Understanding their diverse roles, metabolism, and how their dysregulation contributes to disease is crucial for developing effective diagnostic tools and therapeutic strategies for a wide range of neurological conditions.

The increasing prevalence of neurological conditions demands a better understanding of the biochemical pathogenic mechanisms that underly these disorders. The intricate architecture of the nervous system requires inter- and intracellular signaling mechanisms that are spatially and temporally regulated, often involving the addition of lipid moieties to key proteins. When abnormalities in protein lipidation occur, it affects the localization of important neuronal and glial proteins leading to dysfunction and the development of disease characteristics. Uncovering the mechanisms through which dysregulated protein lipidation leads to pathological sequalae may identify previously unknown or underappreciated targets for treating the disorder. In this session, three accomplished neuroscientists at different stages of career development will provide data from current studies to illustrate the central role that lipid post-translational modifications play in diverse neurological conditions. Specifically, presentations will focus on defining the roles of products of the mevalonate pathway, protein prenylation precursors and cholesterol; regulation of subcellular localization, activity, and signaling in Rho GTPases, and the therapeutic potential of prenyltransferase inhibition in demyelinating disorders.

Nicotinamide adenine dinucleotide (NAD+) is one of the most abundant metabolites in mammalian cells and is crucial to maintain energy homeostasis. NAD+ is also involved in many cellular responses including DNA repair, oxidative stress, Ca2+ signaling, and the circadian rhythm. can be synthesized from three different intracellular pathways, but the NAD+ salvage pathway where nicotinamide phosphoribosyl transferase (NAMPT) is the rate-limiting enzyme, is dominant pathway and generates the largest proportion of NAD+. Impaired NAD+ homeostasis has been observed during aging and in various neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), Parkison’s disease (PD), etc. In this symposium, Dr. Ding will show that MINA, a novel axonal and sensory neuropathy is caused by a genetic variant of NAMPT. Dr. Vargas studied therapeutic potential of NAD+ precursor in ALS mouse model. Dr. Imai is a leader in NAD world and will show data of inter-organ communication to regulate NAD+ metabolism and aging. Dr. Chen is an expert using magnetic resonance imaging (MRI)/spectroscopy (MRS) methodologies and technologies for noninvasively studying cellular metabolism, bioenergetics, function and dysfunction of the brain and other organs. His presentation will focus on whole-brain imaging of NAD at ultrahigh field.

Studies from the four speakers will provide novel mechanistic insights into the roles and therapeutic potentials of NAD-NAMPT axis in CNS diseases. Thus, this symposium will provide a valuable opportunity to learn about the various aspects of NAD metabolism in pathophysiology of CNS diseases and aging and is an excellent example of neurochemistry proposal.

This session will highlight new research in how microglial-mediated neuroinflammation sensitively modulates disease-related pathologies. The underlying theme of the session is microglial processes and pathways that greatly impact brain health. The session will present new findings from a group of researchers that are examining microglial dynamics from different perspectives and using varied strategies to develop exciting new information that impacts a variety of research fields.

The four confirmed speakers are Marie Eve Tremblay, PhD; Marco Colonna, MD; Celeste Karch, PhD; and Michael Nichols, PhD. They will present new data at the ASN 2026 meeting in the areas of microglia stress, dysfunction, inhibition and response to amyloid-beta.

Pain is pervasive throughout society. Opioids are used for the treatment of pain. Increase usage of prescription opioids in addition to diversion of fentanyl and designer opioids has led to an opioid epidemic. New targets for pain and opioid use disorders are required in addition to a molecular understanding of opioid action to functionally separate pain relief from the adverse effects of opioids.

Our session will aim to divulge on this topic through four speakers who are leaders in Chemistry (Susruta Majumdar), Pharmacology (Amynah Pradhan), Neuroscience (Ream Al-Hasani) and Structural Biology (Tao Che) of opioid receptors and opioid alternatives at the Center for Clinical Pharmacology, Washington University School of Medicine, St Louis, MO. Our speakers will cover design of new drugs, novel strategies for treating headache and pain, understanding the endogenous opioid peptide dynamics in fentanyl withdrawal and using cryoEM enabled targeting of allosteric sites in opioid receptors.

This session will be a Concurrent Colloquium on gap junction connectivity in the brain. The theme will be new methods and insights obtained using microscopy and other emerging imaging methods to better understand how astrocytes, neurons, and other cells connect to form distinct reticular networks that interact and have a variety of functions in brain health and disease. Presentations will range from historical perspectives on early use of light microscopy to study gap junctions; to how super-resolution light microscopy is revealing in situ interactions between gap junctions and other organelles in astrocytes, ependymal cells, and tanycytes; the role of gap junctions in intercellular gene regulation as revealed with new spatial multiomics methods; to brain-wide gap junction network mapping. The focus will be on understudied functions and roles of gap junctions beyond direct intercellular channels and new techniques in imaging the cellular connectivity of the brain.

Noncoding RNAs (ncRNAs) represent a diverse class of RNA transcripts that play essential roles in regulating gene expression at both the transcriptional and post-transcriptional levels within the central nervous system (CNS). Growing evidence implicates the dysregulation of ncRNAs in the onset and progression of various neurological and neurodegenerative. This session will explore the emerging functions of ncRNAs in CNS pathophysiology and highlight their increasing potential as diagnostic biomarkers and therapeutic targets.

In a healthy central nervous system, oligodendrocytes are indispensable. These specialized glial cells ensheath neuronal axons with myelin, allowing saltatory conduction of axon potentials, increasing the speed and efficiency of signal transmission. Oligodendrocytes also provide vital metabolic and trophic support to the neurons they myelinate. However, emerging evidence now suggests that oligodendrocytes are not passive victims in neurological decline, but actively contribute to the pathogenesis of a wide range of neurodegenerative diseases, including Alzheimer’s disease, Multiple Sclerosis, and Parkinson’s disease. Furthermore, their dysfunction is implicated in the broader processes of brain aging. This session will discuss new insights into oligodendrocyte pathogenesis across different mouse models, human tissue samples, and in vitro stem cell models. We will explore how oligodendrocytes are altered by neurodegenerative processes and aging, and, critically, how these alterations, in turn, contribute to the progression and severity of these conditions.

Oligodendrocytes form myelin sheath during CNS development (developmental myelination). New concepts have emerged on the role of oligodendroglia and myelination in shaping animal life experience such as motor, cognition, and emotion adaptivity (adaptive myelination). The myelination capacity of oligodendrocytes is controlled by intrinsic molecular programs and extrinsic signals as well from neurons and other glial cell types. Traditionally thought as primary targets in demyelinating disorders, oligodendroglia and myelin damage/injury are also common pathology in neurodegenerative diseases long before neuronal/axonal degeneration and behavioral impairment. It has been increasingly appreciated by the neuroscience community that oligodendroglia and myelin are not simply victims in various CNS pathologies, they are active player in promoting or inhibiting neurodegeneration, neuroinflammation, and others depending on disease/injury contexts, a newly emerging concept of myelination-independent functions of oligodendroglia. Identifying molecular mechanisms (intrinsic and extrinsic) underlying oligodendroglial regulation of CNS pathologies is fundamentally important oligodendroglial biology and will provides novel insights into future therapeutic designs. This symposium will cover recent discoveries or ongoing projects that provide experimental data supporting these newly emerged concepts.

Neurons are highly polarized cells that need to respond to cues in the environment that may differ for distinct subcellular compartments. In order to function properly, neurons must respond accurately to appropriate ligand stimulation that may be initiated at different parts of the neuron. These responses involve trafficking of signaling proteins between the distal axon, soma, and dendritic processes. As axons can extend long distances from the cell bodies, they may experience very different environmental signals that require precise spatiotemporal responses. Distinct signaling pathways may be activated when initiated at the axon compared to the soma that stimulate a coordinated set of trafficking and local translation activities to maintain axonal viability, or initiate a degenerative response. This symposium will include 4 speakers who will discuss axon-specific signaling mechanisms in both peripheral and central neurons, and how they respond to environmental cues including traumatic brain injury and chemotherapeutic treatments.

Emerging data suggests that disruptions of sleep and circadian rhythms may influence the pathogenesis of neurodegenerative diseases. Sleep and the circaidan clock impact many aspects of neurodegenerative pathobiology, including brain metabolism, glial function, protein aggregation, and synaptic integrity. This session will present cutting-edge basic, translational, and clinical research on the mechanisms linking sleep and circadian rhythms to neurodegenerative diseases, particularly Alzheimer and Parkinson diseases. Erik Musiek will discuss molecular mechanisms by which the circadian clock regulates astrocyte and microglial function to impact neurodegenerative pathways in AD and PD mouse models. Shannon Macauley will explore the bidirectional links between brain metabolism, sleep, and AD pathology with a focus on therapeutic intervention. Yo-El Ju will discuss recent data on REM Behavior disorder and other sleep disturbances and their relationship to disease biomarkers and clinical progression to PD in humans. Finally, David Holtzman will speak on the impact of sleep on muitple aspects of tau pathology and tau-mediated neurodegeneration in preclinical models. Ultimately, this session will provide insights into the interplay between sleep, circadian rhythms, and neurodegeneration.

Parkinson’s disease (PD) is a neurodegenerative disorder with a complex etiology. Recent studies suggested multiple PD genes and PD risk genes converge their signaling in regulating synaptic vesicle endocytosis. It remains to be elucidated whether these genes contribute to PD pathogenesis via disrupting synaptic vesicle endocytosis or via other novel signaling mechanisms. This symposium will cover recent advances in pathogenic mechanisms of synaptic endocytic genes including SYNJ1/synaptojanin1, DNAJC6/auxilin1, ITSN1/intersectin1 and LRRK2. Our team is composed of a mixture of junior and senior investigators with diverse research expertise in clinical genetics, bioinformatics, synaptic physiology and cell biology. Together, we will bring latest understandings to the important question of synaptic mechanisms of PD.

This session highlights recent neurotrauma research advances in traumatic brain injuries – TBI, and post-trauma sequala and rehabilitation through collaborative team-based approaches. The central challenge arises from the immense complexity of various TBIs for their pathogenesis and prognosis of post-traumatic sequala. Team science unites basic researchers, translational investigators, physician scientists, as well as content and implementation experts, to address various aspects and impacts of disease in the neurotrauma community, examples of this teamwork integrate the use of complex datasets from both preclinical studies and clinical trials, harmonize protocols and procedures, and use advanced artificial intelligence – AI to understand disease mechanisms, discover precise imaging and biofluid markers, and investigate early treatment and neural cell regeneration for recovery. Dr. Ross Zafonte will overview the advancement and challenges in TBI clinical investigations including TRACK-TBI consortium on post-traumatic sequala assessments. Dr. Zezong Gu will present findings on the chronic impact of TBI on Alzheimer’s disease-related dementias, along insights into the development of the PRECISE-TBI toolkits and using the framework of ODC-TBI for data curation and FAIR practices for future publications. Dr. Kevin Wang will analyze neurotrauma biomarkers in diverse TBI and brain injury animal models from TOP-NT, OBTT, and TAPTE consortia. Dr. Komal Ashraf will share the latest outcomes of complex clinical network and progression of TBI, including post-concussive epilepsy. These ongoing team science interdisciplinary studies, involving both civilian / veteran patients and preclinical models, offer valuable insights into the consequences of neurotrauma to enhance clinical assessments and develop therapeutic strategies.

Chronic pain conditions affect millions of Americans and cost billions to treat annually. Neuroimmune interactions contribute to persistent pain. However, the evidence of peripheral neural and glial mechanisms sustaining primary afferent sensitization has been scarce. In the past few years, significant breakthroughs have been made in peripheral pain mechanisms using single-cell and single-nucleus transcriptome, cell-specific translatome, and epigenome approaches. Recent studies provided a comprehensive overview of peripheral sensory ganglia microenvironment, including revealing cell types and subtypes, deciphering intercellular communications, and probing the cell subtype-specific function in chronic pain conditions. Cross-species transcriptome profile comparison has been made between human and mouse sensory ganglia (including dorsal root ganglia and trigeminal ganglia), offering important perspectives in translational pain research. Sex-specific pain mechanisms were revealed, which highlighted the need for personalized treatment approaches. The contribution of specific glial cell types such as satellite glial cells and resident macrophages are under intense interrogation. This proposed symposium is organized by Dr. Alison Xie, who pioneered the studies on the roles of satellite glial cells in chronic pain, and will host four world-leading scientists in the fields of pain, glial biology, and neuroimmunology. Presentations will focus on their recently published (2024-2026) and unpublished work in sensory ganglia omics and pain mechanistic studies. All invitations have been confirmed.

Neurodegenerative and neuropsychiatric diseases such as ALS, frontotemporal dementia (FTD), NeuroHIV, and depression are recognized as disorders of both neuronal dysfunction and immune dysregulation. This symposium will focus on the integration of patient-derived cellular systems with neuroimmune research to elucidate how inflammatory and glial signaling contribute to disease progression. Talks will explore how blood-derived cells from patients are being used to identify disease-specific immune phenotypes, and how associated patient data are analyzed using advanced biostatistics. Using iPSC-derived models, speakers will also present data defining mechanisms by which immune cells and cytokine networks shape neuronal health. By advancing our understanding of how neuroimmune interactions are altered in patient-specific contexts utilizing cellular, molecular, and systems-level approaches, this session aims to highlight novel, targetable pathways and drive forward the development of precision medicine in translational neurobiology.

Our session will represent individuals with a range of global backgrounds, and who are all successful and dynamic women in science. Dr. Matt, co-chair, will discuss her work on inflammatory signaling and viral kinetics in iPSC-derived models and clinical samples of patients with HIV and depression. Dr. Jensen, co-chair, will discuss regional astrocytic impacts on neuronal health and survival in the context of ALS and FTD. Dr. Bekhbat will discuss data from depressed patients linking monocyte metabolism with inflammation-sensitive behaviors related to reward and energy. Dr. Dastgheyb has been approached for inclusion but has not yet confirmed. Tentatively, she would round out the session with discussion of biostatistical analysis of cohort samples.