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VEGF counteracts amyloid-β-induced synaptic dysfunction.

Laurent Martin1, Pauline Bouvet1, Naura Chounlamountri1

  • 1Institut NeuroMyoGène (INMG), Synaptopathies and Autoantibodies, Institut National de la Santé et de la Recherche Médicale (INSERM), U1217, Centre National de la Recherche Scientifique (CNRS) UMR5310, 69000 Lyon, France; Université Claude Bernard Lyon 1, 69000 Lyon, France.

Cell Reports
|May 12, 2021
PubMed
Summary
This summary is machine-generated.

Vascular endothelial growth factor (VEGF) accumulates with amyloid-beta plaques in Alzheimer

Keywords:
AlzheimerVEGFamyloid-beta oligomersamyloid-beta peptideglutamate receptorslong-term potentiationsynapsesynaptic transmission

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Alzheimer's disease (AD) involves synaptic dysfunction driven by amyloid-beta oligomers (Aβo).
  • The vascular endothelial growth factor (VEGF) pathway is crucial for synapse function.
  • VEGF pathway alterations are implicated in early-stage AD pathogenesis.

Purpose of the Study:

  • To investigate the interaction between VEGF and Aβo in Alzheimer's disease.
  • To determine the impact of this interaction on neuronal signaling and synaptic function.
  • To explore the therapeutic potential of restoring VEGF signaling in AD.

Main Methods:

  • Analysis of postmortem human AD brains and APP/PS1 mouse models.
  • Identification of Aβo-VEGF binding domains.
  • Assessment of VEGFR2 activation, synaptic transmission, long-term potentiation (LTP), long-term depression (LTD), and dendritic spine morphology.
  • Investigation of the caspase-3-calcineurin pathway.

Main Results:

  • VEGF accumulates in and around amyloid plaques in AD brains and mouse models.
  • Direct interaction between Aβo and VEGF impairs VEGFR2 activation in neurons.
  • VEGF gain of function rescued synaptic transmission, LTP, and dendritic spines, while blocking Aβo-induced LTD.
  • VEGF inhibits the caspase-3-calcineurin pathway, preventing Aβo-induced glutamate receptor loss.

Conclusions:

  • The VEGF pathway is significantly altered in Alzheimer's disease.
  • Aβo directly interacts with VEGF, disrupting neuronal signaling and synaptic function.
  • Restoring VEGF signaling presents a potential therapeutic strategy for rescuing synaptic dysfunction in AD.