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Basic Science and Pathogenesis.

Stefan Wendt1, Ada J Lin1, Sarah N Ebert1

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

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
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Microglia can protect against early Alzheimer's disease (AD) pathology in a 3D human model, but their effectiveness diminishes with severe amyloid-beta (Aβ) exposure. This model aids in identifying new therapeutic targets for AD.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Genomics

Background:

  • Alzheimer's disease (AD) involves amyloid-beta (Aβ) plaques, but the role of microglia in neurodegeneration remains unclear.
  • Microglial function in AD can be either protective or detrimental depending on disease stage.

Purpose of the Study:

  • To characterize microglial responses to Aβ pathology using a novel 3D human induced pluripotent stem cell (iPSC)-derived neurosphere model.
  • To investigate the impact of microglia on neuronal health and gene expression in the context of Aβ-induced amyloidosis.

Main Methods:

  • Developed a 60-day 3D neurosphere model using iPSC-derived neurons and microglia.
  • Induced amyloidosis with continuous synthetic oligomeric Aβ treatment.
  • Monitored neuronal oxidative stress and calcium activity using roGFP1 and GCaMP6f sensors.
  • Analyzed transcriptomic changes via single-nuclei RNA sequencing (snRNA-seq).

Main Results:

  • Microglia infiltrated neurospheres and prevented neurotoxicity in mild Aβ exposure (3 weeks).
  • Microglia failed to prevent neurotoxicity in severe Aβ exposure (5 weeks).
  • snRNA-seq revealed microglia modulated oxidative stress genes and AD-associated genes (APOE, CLU, FTL) in astrocytes and neurons.
  • Microglia showed enhanced Aβ clearance after anti-Aβ antibody treatment.

Conclusions:

  • The 3D neurosphere model effectively mimics key Alzheimer's disease pathological features.
  • Microglia exhibit neuroprotective properties in this model, potentially enhanced by antibody treatment.
  • Microglia are critical in driving AD-associated transcriptomic changes under severe Aβ insult, highlighting their complex role and therapeutic potential.