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Lymphocyte activation gene 3 (LAG3) drives Parkinson's disease pathology by mediating alpha-synuclein propagation. Blocking LAG3 in neurons reduces pathology and neurodegeneration, offering a new therapeutic target.

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Lymphocyte activation gene 3 (LAG3) is implicated in the spread of pathological proteins in Parkinson's disease (PD).
  • Alpha-synuclein (αSyn) preformed fibrils (PFFs) are key drivers of PD pathology.
  • Understanding the role of neuronal LAG3 in αSyn propagation is crucial for developing effective PD therapies.

Purpose of the Study:

  • To investigate the role of neuronal LAG3 in the binding, uptake, and propagation of αSyn PFFs.
  • To determine if targeting neuronal LAG3 can mitigate PD-associated pathology and neurodegeneration.

Main Methods:

  • Utilized neuronal LAG3 conditional knockout mice and human induced pluripotent stem cells-derived dopaminergic (DA) neurons.
  • Performed electrophysiological recordings to assess neuronal activity.
  • Administered an anti-human LAG3 antibody to human DA neurons treated with αSyn PFFs.

Main Results:

  • Absence of neuronal LAG3 significantly reduced αSyn pathology, motor dysfunction, and neurodegeneration in vivo.
  • αSyn PFFs induced neuronal hyperactivity in wild-type neurons, an effect resisted by LAG3-deficient neurons.
  • Anti-human LAG3 antibody treatment inhibited αSyn PFF binding and uptake in human DA neurons.

Conclusions:

  • Neuronal LAG3 is essential for mediating αSyn propagation and associated pathological disruptions in Parkinson's disease.
  • Targeting LAG3 presents a promising therapeutic strategy for PD and other alpha-synucleinopathies.
  • LAG3 blockade effectively prevents αSyn pathology spread and neurotoxicity.