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Basic Science and Pathogenesis.

Margaret M Tish1, Lauren Gao1, Zihui Ou1

  • 1Emory University School of Medicine, Atlanta, GA, USA.

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|December 23, 2025
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Summary
This summary is machine-generated.

Human locus coeruleus (LC) organoids model Alzheimer's disease (AD) by showing early tau pathology. These organoids reveal how LC degeneration impacts noradrenergic transmission in AD.

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Area of Science:

  • Neuroscience
  • Stem Cell Biology
  • Alzheimer's Disease Research

Background:

  • The locus coeruleus (LC) is the first brain region affected by tau pathology in Alzheimer's disease (AD) and degenerates significantly.
  • Dysregulation of norepinephrine (NE) transmission from the LC is linked to AD symptoms, affecting cognition and memory.
  • Current understanding of LC in AD relies on indirect models; direct study of early human LC pathology is lacking.

Purpose of the Study:

  • To create and characterize human locus coeruleus (LC) organoids that mimic LC-like noradrenergic neurons.
  • To investigate early pathological changes in human LC neurons derived from familial Alzheimer's disease (AD) mutation carriers.
  • To compare gene expression and tau pathology in AD-derived LC organoids versus controls.

Main Methods:

  • Generation of LC organoids from human induced pluripotent stem cells (iPSCs) from familial AD patients and healthy controls.
  • Characterization of organoids using high-performance liquid chromatography (HPLC), immunohistochemistry, RNA-scope, and RNA-sequencing.
  • Comparison with human cortical organoids to validate LC-specific features.

Main Results:

  • LC organoids successfully replicated key features of human LC neurons, including NE and dopamine production and specific protein/mRNA expression.
  • Transcriptomic analysis confirmed LC organoids closely resemble the human LC, with AD-derived organoids showing altered gene expression linked to AD pathophysiology.
  • Familial AD LC organoids exhibited an increased 4R:3R tau ratio, indicating early pathogenic tau alterations.

Conclusions:

  • Human LC organoids serve as a viable model for studying LC-like noradrenergic neurons and their role in AD.
  • These organoids demonstrate that familial AD mutations lead to pathogenic alterations in LC neurons, including abnormal tau processing.
  • Further study of these organoids offers novel insights into LC vulnerability and AD pathogenesis.