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Related Experiment Video

Updated: Jan 8, 2026

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Basic Science and Pathogenesis.

Wonyoung Koh1, Gwang-Hyun Park1, Yoomin Park1

  • 1GradiantBioconvergence, Songpa-Gu, Seoul, Korea, Republic of (South).

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Summary

This study developed a 3D Alzheimer's disease (AD) organoid model with microglia to study neuroinflammation. The model successfully mimicked AD inflammatory responses and showed potential for drug screening.

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Area of Science:

  • Neuroscience
  • Stem Cell Biology
  • Disease Modeling

Background:

  • Alzheimer's disease (AD) pathology involves amyloid-β plaques, tau protein, and neuroinflammation.
  • Induced pluripotent stem cell (iPSC) technology enables 3D cerebral organoid generation, improving human neurodevelopmental modeling.
  • Integrating microglia into organoids mimics the AD brain's inflammatory environment, aiding study of microglial-neuronal interactions.

Purpose of the Study:

  • To establish a physiologically relevant co-culture system of cerebral organoids and microglia.
  • To investigate neuroinflammation in Alzheimer's disease using patient-derived iPSCs.
  • To create a platform for identifying therapeutic targets for AD.

Main Methods:

  • Generated cerebral organoids and microglia from healthy control and AD patient-derived iPSCs.
  • Autologously co-cultured organoids and microglia to maintain donor specificity.
  • Induced neuroinflammation using lipopolysaccharide (LPS) and evaluated a JNK inhibitor (SP600125).

Main Results:

  • LPS treatment induced pro-inflammatory cytokine release (TNF-α, IL-6, IL-1β) only in co-cultures with microglia.
  • The JNK inhibitor SP600125 significantly reduced pro-inflammatory cytokine levels.
  • Microglia demonstrated amyloid-β phagocytosis, and co-cultures showed altered amyloid-β levels compared to organoids without microglia.

Conclusions:

  • Co-culturing organoids and microglia at a developmentally analogous timepoint creates a more physiologically relevant system than traditional models.
  • This iPSC-based platform successfully recapitulates AD-associated inflammatory phenotypes.
  • The developed platform is valuable for mechanistic studies and drug screening in Alzheimer's disease research.