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Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
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Amyloid-β plaques disrupt axon initial segments.

Miguel A Marin1, Jokubus Ziburkus2, Joanna Jankowsky1

  • 1Department of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

Experimental Neurology
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Alzheimer's disease (AD) amyloid-β plaques disrupt neuron structure. Near plaques, axon initial segments (AIS) decrease in density and length, potentially impairing brain function.

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Alzheimer'sAxonDegenerationIon channel

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Amyloid-β (Aβ) plaques are a hallmark of Alzheimer's disease (AD), linked to synaptic dysfunction and cognitive decline.
  • Axon initial segments (AIS) are critical for neuronal excitability and polarity, but their structural integrity near Aβ plaques is not well understood.

Purpose of the Study:

  • To investigate the impact of Aβ plaques on the structure of axon initial segments (AIS) in a mouse model of AD.

Main Methods:

  • Utilized a mouse model of AD with varying plaque loads.
  • Quantified AIS density and length in proximity to fibrillar, thioflavin-labeled Aβ plaques.
  • Assessed microglial density near plaques.

Main Results:

  • Observed a significant decrease in AIS density up to 75μm from Aβ plaques in animals with moderate and severe plaque loads.
  • Found increased microglial densities surrounding the plaques.
  • Demonstrated significantly reduced AIS lengths adjacent to Aβ plaques in animals with severe plaque loads.

Conclusions:

  • Aβ plaques disrupt the structure of AIS in the local brain environment.
  • AIS loss near plaques is a potential consequence of AD pathology that may significantly impact neuronal function and contribute to cognitive deficits.