Selected Colloquium
Session Room 220
Session Room 220
Tuesday, June 17, 12:15 PM – 01:15 PM
Selected Colloquium 3: Targeting NMDA Receptors Mediate Neuron-Glia Interactions for the Treatment of Neuropsychiatric Disorders: From Basic Research to Application
Excitatory neurotransmission via N-methyl-D-aspartate receptors (NMDARs), a key subtype of glutamate receptors, is crucial for numerous functions in the mammalian brain, including neuronal plasticity, learning, and memory. Moreover, NMDARs play a pivotal role in the pathology of numerous neuropsychiatric disorders. Traditionally, neuroscience has predominantly focused on neurons, shaping our understanding of psychiatric conditions within a neuron-centric framework. However, the essential role of glial cells—such as astrocytes, oligodendrocytes, and microglia—in maintaining and modulating brain function is increasingly recognized. These glial cells, which outnumber neurons, are integral to the integration and functionality of the central nervous system.
This evolving perspective emphasizes the necessity of investigating neuron-glial interactions to attain a comprehensive understanding of neurobiological processes and psychiatric disorders, including Alexander disease, multiple sclerosis, depression, and schizophrenia. Taking schizophrenia as an example, this severe mental disorder affects approximately 1% of the global population and illustrates the complexities of understanding and treating neuropsychiatric conditions. Characterized by a spectrum of positive and negative symptoms, along with cognitive deficits, schizophrenia has seen limited therapeutic advancements over the past six decades. Notably, the negative symptoms and cognitive impairments highlight the need for innovative treatment strategies. Recent evidence supports the NMDAR hypofunction hypothesis, wherein NMDAR blockade induces symptoms akin to those of schizophrenia. Emerging therapies aimed at enhancing NMDAR function, particularly those targeting the glycine modulatory site (GMS) on NMDARs, show promise in alleviating schizophrenia symptoms. D-amino acid oxidase (DAO), which metabolizes D-serine—a critical co-agonist at the GMS of NMDARs—has become a focal point for novel treatment development. Strategies that target the GMS of NMDARs, either directly or indirectly by enhancing synaptic glycine/D-serine levels through astrocytic or other glial modulation, represent a promising avenue for addressing the needs of patients with schizophrenia and related neuropsychiatric disorders.
In response to these urgent medical challenges, this symposium will explore the role of NMDARs and neuron-glia interactions in preclinical models, with a brief extension to clinical trials. We are pleased to feature four distinguished speakers from Japan, Korea, Malaysia, and Taiwan. Professor Schuichi Koizumi from Yamanashi GLIA Center will commence the symposium with insights into "gliotransmitters" and neuron-to-glia communication in both physiological and pathological contexts (references #1 & #2). Dr. Jungjoo Park, a postdoctoral researcher at IBS in Korea, will present her findings on glial phagocytosis in multiple sclerosis (references #3 & #4). Dr. Tomoko Soga, Director of Animal Research Platform at Monash University Malaysia, will discuss key molecules involved in neuron-glia interactions during stress (references #5 & #6). Finally, Professor Wen-Sung Lai from National Taiwan University will introduce a novel DAO inhibitor and its potential for treating schizophrenia and multiple system atrophy (MSA), concluding with an update on an ongoing clinical trial in MSA (references #7 & #8). Together, this symposium aims to illuminate the significance of neuron-glia interactions and provide critical insights for developing novel therapeutic strategies to address unmet needs in neuropsychiatric disorders.
This evolving perspective emphasizes the necessity of investigating neuron-glial interactions to attain a comprehensive understanding of neurobiological processes and psychiatric disorders, including Alexander disease, multiple sclerosis, depression, and schizophrenia. Taking schizophrenia as an example, this severe mental disorder affects approximately 1% of the global population and illustrates the complexities of understanding and treating neuropsychiatric conditions. Characterized by a spectrum of positive and negative symptoms, along with cognitive deficits, schizophrenia has seen limited therapeutic advancements over the past six decades. Notably, the negative symptoms and cognitive impairments highlight the need for innovative treatment strategies. Recent evidence supports the NMDAR hypofunction hypothesis, wherein NMDAR blockade induces symptoms akin to those of schizophrenia. Emerging therapies aimed at enhancing NMDAR function, particularly those targeting the glycine modulatory site (GMS) on NMDARs, show promise in alleviating schizophrenia symptoms. D-amino acid oxidase (DAO), which metabolizes D-serine—a critical co-agonist at the GMS of NMDARs—has become a focal point for novel treatment development. Strategies that target the GMS of NMDARs, either directly or indirectly by enhancing synaptic glycine/D-serine levels through astrocytic or other glial modulation, represent a promising avenue for addressing the needs of patients with schizophrenia and related neuropsychiatric disorders.
In response to these urgent medical challenges, this symposium will explore the role of NMDARs and neuron-glia interactions in preclinical models, with a brief extension to clinical trials. We are pleased to feature four distinguished speakers from Japan, Korea, Malaysia, and Taiwan. Professor Schuichi Koizumi from Yamanashi GLIA Center will commence the symposium with insights into "gliotransmitters" and neuron-to-glia communication in both physiological and pathological contexts (references #1 & #2). Dr. Jungjoo Park, a postdoctoral researcher at IBS in Korea, will present her findings on glial phagocytosis in multiple sclerosis (references #3 & #4). Dr. Tomoko Soga, Director of Animal Research Platform at Monash University Malaysia, will discuss key molecules involved in neuron-glia interactions during stress (references #5 & #6). Finally, Professor Wen-Sung Lai from National Taiwan University will introduce a novel DAO inhibitor and its potential for treating schizophrenia and multiple system atrophy (MSA), concluding with an update on an ongoing clinical trial in MSA (references #7 & #8). Together, this symposium aims to illuminate the significance of neuron-glia interactions and provide critical insights for developing novel therapeutic strategies to address unmet needs in neuropsychiatric disorders.
12:15 PM – 12:35 PM
20 min
20 min