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Basic Science and Pathogenesis.

Keith P Smith1, Taylor A Strope2,3, Brittany M Hauger3

  • 13901 rainbow blvd, Kansas City, KS, USA.

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Summary
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Mitochondrial dysfunction is prominent in Down Syndrome-associated Alzheimer's Disease (DSAD), with increased amyloid precursor protein (APP) in brain mitochondria. This pathology is mirrored in DSAD cerebral organoid models.

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Area of Science:

  • Neuroscience
  • Genetics
  • Cell Biology

Background:

  • Alzheimer's disease (AD) is characterized by mitochondrial dysfunction and amyloid-beta (Aβ) accumulation.
  • The pathological role of these hallmarks in Down Syndrome-associated Alzheimer's Disease (DSAD) remains unclear.

Purpose of the Study:

  • To investigate mitochondrial function, Aβ accumulation, and APP localization in DSAD.
  • To compare DSAD pathologies with sporadic AD (sAD) and Down Syndrome (DS) without AD.

Main Methods:

  • Analysis of postmortem brain tissue from DSAD, DS, and non-DS (ND) individuals.
  • Utilized human induced pluripotent stem cell (iPSC) models differentiated into cerebral organoids.
  • Assessed mitochondrial function via Seahorse XF analyzer, protein levels via Western Blotting, and Aβ via ELISA.
  • Performed proteomic analysis on brain and mitochondrial samples.

Main Results:

  • DSAD brain tissue exhibited significantly reduced mitochondrial function and increased full-length APP in mitochondria.
  • Mitochondrial dysfunction in DSAD was more severe than in sAD.
  • Cerebral organoid models recapitulated DSAD phenotypes, including increased mitochondrial APP and impaired mitochondrial function.
  • Proteomics revealed differential expression of inflammatory and mitochondrial pathways in DSAD.

Conclusions:

  • DSAD is characterized by profound mitochondrial dysfunction in the brain, which is reproducible in cerebral organoid models.
  • Increased APP accumulation within mitochondria is a key feature of DSAD pathology.