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Basic Science and Pathogenesis.

Printha Wijesinghe1, Amir Hosseini1, Matthew Campbell1

  • 1The University of British Columbia, Vancouver, BC, Canada.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
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Alzheimer's disease (AD) disrupts clearance mechanisms in the retina, impairing glymphatic drainage and macrophage function. This study reveals these disruptions using novel 3D retinal imaging, offering insights into AD pathogenesis.

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Area of Science:

  • Neuroscience
  • Ophthalmology
  • Pathology

Background:

  • Alzheimer's disease (AD) pathogenesis involves an imbalance in amyloid-beta (Aβ) production and clearance.
  • The inner blood-retina barrier (iBRB) serves as a functional analog to the blood-brain barrier (BBB), making it a valuable model for studying AD-related clearance mechanisms.
  • Investigating cellular interactions at the iBRB, including neuronal and glial cells, retinal vasculature, and macrophages, is crucial for understanding AD.

Purpose of the Study:

  • To investigate impaired Aβ clearance mechanisms in Alzheimer's disease (AD) using the inner blood-retina barrier (iBRB) as a model.
  • To examine the interactions among neuronal and glial cells, retinal vasculature, and blood-derived macrophages in AD pathogenesis.
  • To apply novel three-dimensional (3D) ex vivo retinal imaging for studying clearance processes at the iBRB.

Main Methods:

  • Analysis of wholemount neuroretinas from human AD donors and controls, and retinal cross-sections from APP-PS1 mice and controls.
  • Utilized three- and two-dimensional ex vivo retinal imaging techniques.
  • Employed immunolabeling for Aβ peptides, soluble Aβ oligomers (SAβOs), microglia/macrophages (IBA1), macroglia (GFAP, GS), aquaporin-4 (AQP4), and retinal blood vessel endothelium (UEA-1).

Main Results:

  • Human AD neuroretinas showed increased Aβ deposits and microglia/macrophages (IBA1+), with reduced levels of glymphatic drainage markers (GFAP, GS, AQP4).
  • Clearance of soluble Aβ oligomers (SAβOs) by peripheral macrophage-like monocytes was significantly diminished in AD retinas.
  • Mouse models exhibited increased GFAP, AQP4, and IBA1, alongside elevated APP/Aβ peptides, indicating gliosis and impaired clearance systems.

Conclusions:

  • Wholemount analysis revealed that glymphatic clearance and microglial phagocytosis are compensatory mechanisms disrupted in AD.
  • Peripheral macrophage-like monocytes play a role in SAβO clearance in controls, a function impaired in AD.
  • Ex vivo 3D retinal imaging offers novel insights into iBRB and BBB analog processes in AD pathogenesis.