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This joint seminar explores the critical role of neuroglial communication in Central Nervous System (CNS) degeneration. Featuring distinguished researchers Dr. Eric Boué-Grabot and Dr. David Blum, the session will delve into novel therapeutic targets and the underlying cellular mechanisms of major neurodegenerative diseases, specifically Amyotrophic Lateral Sclerosis (ALS) and Alzheimer's Disease (AD).
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Event Details
• Date: June 10th, 2026
• Time: 16:00~17:00
• Venue: Teaching & Research Building, Room 1801, ShuanHo Campus
• Organizer: TMU Biomedical Engineering
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Speaker 1: Eric Boué-Grabot, PhD / Directeur de Recherche CNRS, Université de Bordeaux - CNRS
Title: Neuronal versus Microglial P2X4 Receptors in CNS Disease: Lessons from Amyotrophic Lateral Sclerosis
Short Summary: P2X receptors are ATP-gated cation channels that contribute to brain signaling by mediating the effects of extracellular ATP released by neurons and glial cells. This talk will focus on P2X4 receptors, whose surface expression is tightly controlled under physiological conditions but markedly altered in several CNS diseases, including ischemia, chronic pain, epilepsy, multiple sclerosis, and neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD).
Using ALS as a central example, recent findings obtained with genetic mouse models (including P2X4KI and P2X4KO mice crossed with SOD1 ALS mice) will be presented. These data reveal that P2X4 receptors play cell-specific and opposing roles in ALS. Microglial P2X4 appears to slow disease progression, motoneuron degeneration, spinal microgliosis, peripheral nerve macrophage infiltration, and death. In contrast, neuronal P2X4 accelerates disease progression and reduces survival. These findings highlight P2X4 as a context-dependent regulator of neuroinflammation and neurodegeneration, and suggest that future therapeutic strategies should consider the cellular and temporal specificity of P2X4 signaling.
Key Messages:
• P2X4 receptors are tightly regulated under physiological conditions but become dysregulated in CNS diseases.
• In ALS, P2X4 does not have a uniform role: its impact depends on the cell type in which it is expressed.
• Microglial P2X4 exerts a protective effect by slowing neuroinflammation, motoneuron degeneration, and disease progression.
• Neuronal P2X4 has a deleterious effect, accelerating disease progression and death.
• Targeting P2X4 in ALS will require cell-specific and stage-specific therapeutic approaches rather than global receptor activation or inhibition.
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Speaker 2: David Blum, PhD / Directeur de Recherche Inserm, Inserm UMR-S1172
Title: The purinergic neuroglial link to brain plasticity and neurodegeneration
Abstract: Epidemiological and experimental studies support the beneficial effect of habitual caffeine (aka theine) consumption in Alzheimer's Disease (AD). The underlying mechanisms remain however ill-defined but are thought to depend on its ability to block adenosine A2A receptors, found upregulated in hippocampal neurons and astrocytes of AD patients. The present seminar will highlight data from our group that support that the modulation of the A2A receptor impacts neuroglial regulation and memory deficits in models of Alzheimer's Disease. Based on these experimental data, current and expected translational development will be discussed.
Key Messages:
• Caffeine and its ability to block adenosine receptors is of clinical interest in Alzheimer's Disease and Tauopathies.
• Mechanisms remain to be fully uncovered but apparently involve reshaping of neuro-glial communication.
• Clinical and bioengineering development are needed to fully understand their clinical impact.
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