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Tau association with synaptic vesicles causes presynaptic dysfunction.

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Pathological Tau protein directly binds to synaptic vesicles, impairing neurotransmission in neurons. This early synaptic dysfunction in tauopathies may offer new therapeutic targets for neurodegenerative diseases.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Tau protein is linked to over 20 neurodegenerative diseases, including Alzheimer's disease.
  • Pathological Tau detaches from microtubules and mislocalizes to synapses, causing early synaptic dysfunction before aggregate formation.
  • The precise mechanism of early synaptic impairment in tauopathies remains unclear.

Purpose of the Study:

  • To investigate the mechanism by which pathological Tau impairs synaptic function.
  • To determine if Tau's interaction with synaptic vesicles is critical for its presynaptic toxicity.
  • To explore therapeutic strategies targeting Tau-vesicle binding.

Main Methods:

  • Utilized fly and rat neuronal models.
  • Investigated the binding interaction between pathogenic Tau and synaptic vesicles using its N-terminal domain.
  • Assessed the impact of Tau on synaptic vesicle mobility and neurotransmitter release rate.
  • Examined Tau mutants lacking vesicle binding domains.
  • Tested a membrane-permeable peptide to block Tau-vesicle binding in rat neurons.

Main Results:

  • Pathogenic Tau binds to synaptic vesicles via its N-terminal domain.
  • This binding interferes with presynaptic functions, reducing synaptic vesicle mobility and release rate, thereby lowering neurotransmission.
  • Tau mutants unable to bind vesicles did not impair synaptic function in fly neurons.
  • A peptide blocking Tau-vesicle binding ameliorated Tau-induced synaptic toxicity in rat neurons.

Conclusions:

  • Pathological Tau directly impairs presynaptic function through binding to synaptic vesicles.
  • This interaction represents a key mechanism underlying early synaptic dysfunction in tauopathies.
  • Targeting Tau-vesicle binding presents a potential therapeutic avenue for neurodegenerative diseases involving Tau.