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Microglia express higher levels of lymphocyte activation gene 3 (Lag3) than neurons, yet the contribution of microglial Lag3 to \u03b1-syn recognition, glial crosstalk, and neurodegeneration is unknown.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>\n                    Biochemical binding assays, live-cell imaging, cytokine profiling, and neuron\u2013microglia\u2013astrocyte co-culture paradigms were used to define Lag3-dependent \u03b1-syn preformed fibril (PFF) binding, uptake, and microglial activation. To interrogate in vivo function, microglia-specific Lag3 conditional knockout mice (Lag3\n                    <jats:sup>L\/L<\/jats:sup>\n                    -Cx3cr1\n                    <jats:sup>CreER<\/jats:sup>\n                    ) and littermate controls received unilateral intrastriatal \u03b1-syn PFF injections, followed by histological, biochemical, and behavioral assessments of \u03b1-syn pathology, gliosis, nigrostriatal integrity, and motor performance.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\u03b1-syn PFFs bound microglial Lag3 with high specificity and nanomolar affinity and required Lag3 for efficient fibril internalization and induction of proinflammatory cytokines. Microglial Lag3 deficiency markedly blunted \u03b1-syn PFF\u2013evoked microglial activation, prevented cytokine-driven conversion of astrocytes into neurotoxic reactive A1 astrocytes, and abolished astrocyte-dependent neuronal death in vitro. In vivo, microglia-specific Lag3 deletion reduced cortical, striatal, and substantia nigra pS129 \u03b1-syn pathology, suppressed microgliosis and A1 astrocyte induction, preserved substantia nigra dopaminergic neurons and striatal dopamine transporter\/tyrosine hydroxylase expression, and ameliorated \u03b1-syn PFF\u2013induced motor deficits.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>This study identifies microglial Lag3 as a key receptor linking extracellular \u03b1-syn PFF recognition to inflammatory amplification, neurotoxic reactive A1 astrocyte conversion, and dopaminergic neurodegeneration. Together with prior work on neuronal Lag3, these findings support a cell-type\u2013specific dual-axis model in which neuronal Lag3 mediates \u03b1-syn propagation while microglial Lag3 drives glia-dependent neurotoxicity, positioning Lag3 as a promising precision therapeutic target in \u03b1-synucleinopathies.<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.01.06.697996","type":"posted-content","created":{"date-parts":[[2026,1,7]],"date-time":"2026-01-07T08:55:12Z","timestamp":1767776112000},"source":"Crossref","is-referenced-by-count":2,"title":["Microglial Lag3 Drives \u03b1-Synuclein\u2013induced Neurotoxic Activated (A1) Astrocytes and Neurodegeneration"],"prefix":"10.64898","author":[{"given":"Xiuli","family":"Yang","sequence":"first","affiliation":[{"name":"Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA"},{"name":"Department of Neurology, Johns Hopkins University School 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