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    Rett Syndrome (RTT) involves astrocyte dysfunction. Reducing astrocyte SEMA3C protein in RTT models improves neuronal connections and motor function, suggesting a therapeutic target.

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    Area of Science:

    • Neuroscience
    • Developmental Biology
    • Genetics

    Background:

    • Astrocytes normally support neuronal connectivity during development.
    • Rett Syndrome (RTT) disrupts neurodevelopment, causing motor, sensory, and cognitive deficits.
    • RTT astrocytes inhibit wildtype neuron outgrowth, indicating problematic secreted factors.

    Purpose of the Study:

    • Identify specific astrocyte-secreted factors contributing to RTT pathology.
    • Investigate the role of class 3 semaphorin SEMA3C in RTT.
    • Determine the therapeutic potential of targeting astrocyte SEMA3C in RTT.

    Main Methods:

    • Utilized astrocyte and neuron cell cultures to assess SEMA3C function.
    • Employed genetic reduction of astrocyte SEMA3C in RTT model mice.
    • Analyzed dendritic arborization, synaptic activity, visual acuity, and motor behavior.

    Main Results:

    • SEMA3C, secreted at higher levels by RTT astrocytes, inhibits dendrite outgrowth via PLXND1/NRP2.
    • Reducing astrocyte SEMA3C in RTT mice improved dendritic complexity and normalized synaptic function.
    • Astrocyte SEMA3C reduction ameliorated RTT-associated visual and motor deficits in mice.

    Conclusions:

    • Astrocyte-secreted SEMA3C contributes significantly to RTT pathology.
    • The SEMA3C-NRP2-PLXND1 pathway is implicated in RTT pathogenesis.
    • Targeting astrocyte SEMA3C presents a potential therapeutic strategy for RTT and related neurodevelopmental disorders.