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Autoantibodies to synapsin I sequestrate synapsin I and alter synaptic function.

Anna Rocchi1,2, Silvio Sacchetti1, Antonio De Fusco1,3

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Autoantibodies targeting Synapsin I (SynI) impair neuronal function by reducing synapses and disrupting synaptic transmission. These findings reveal a mechanism for autoimmune neurological diseases involving intracellular autoantigens.

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Synapsin I (SynI) is crucial for synaptic vesicle trafficking.
  • Autoantibodies against SynI are found in neurological diseases, but their neuronal effects are unknown.

Purpose of the Study:

  • To investigate the effects and fate of autoantibodies against Synapsin I in neurons.
  • To determine if SynI autoantibodies contribute to autoimmune neurological diseases.

Main Methods:

  • Primary hippocampal neurons were exposed to patient autoantibodies or purified SynI antibodies.
  • SynI knockout neurons were used to confirm specificity.
  • Internalization and intracellular fate of antibodies were analyzed.

Main Results:

  • Patient autoantibodies to SynI reduced synapse density and impaired synaptic transmission (glutamatergic and GABAergic).
  • These effects were replicated with purified antibodies and absent in SynI knockout neurons.
  • Autoantibodies were internalized, interacted with SynI, causing aggregation and reducing synaptic vesicle density.

Conclusions:

  • Autoantibodies against intracellular SynI can reach and inactivate their target within neurons.
  • Antibody-mediated synaptic dysfunction contributes to autoimmune neurological diseases associated with SynI autoantibodies.