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    Area of Science:

    • Neuroscience
    • Proteomics
    • Synaptic Biology

    Background:

    • Neuronal connection dysfunction contributes to cognitive deficits in mental disorders.
    • Synaptic proteins, shed into cerebrospinal fluid (CSF), regulate cognitive processes.
    • The therapeutic potential of soluble synaptic proteins for brain disorders is largely unexplored.

    Purpose of the Study:

    • To identify shed synaptic proteins dysregulated in schizophrenia (SCZ) CSF using quantitative proteomics.
    • To investigate the role and therapeutic potential of a specific downregulated protein, α2δ-1, in cognitive dysfunction.

    Main Methods:

    • Quantitative proteomics analysis of CSF from SCZ subjects.
    • Characterization of soluble α2δ-1 release and function in neuronal networks.
    • Assessment of synthetic soluble α2δ-1 efficacy in a mouse model of SCZ.

    Main Results:

    • Soluble α2δ-1 was significantly reduced in SCZ CSF and other brain disorder CSF proteomes.
    • Brain releases soluble α2δ-1 in an activity-dependent manner, influencing neuronal network dynamics.
    • Administration of synthetic soluble α2δ-1 ameliorated cognitive and interneuron deficits in a mouse model.

    Conclusions:

    • Reduced soluble α2δ-1 is a potential biomarker for SCZ and other brain disorders.
    • Soluble α2δ-1 plays a role in regulating neuronal plasticity and network function.
    • Shed synaptic proteins, like α2δ-1, represent promising therapeutic targets for cognitive enhancement in brain disorders.