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Basic Science and Pathogenesis.

Caitlin S Latimer1, Miranda E Orr2,3, Emily E Killingbeck Schneidereit4

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Vervet monkeys, a model for early Alzheimer's disease (AD), show amyloid-beta plaques linked to specific molecular changes. This study reveals cell-type-specific alterations in the brain, offering new therapeutic targets for AD.

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Area of Science:

  • Neuroscience
  • Primate Models
  • Alzheimer's Disease Research

Background:

  • Vervet monkeys (Chlorocebus aethiops) exhibit early Alzheimer's disease (AD) pathology, including amyloid-beta (Aβ) deposition without neurofibrillary tangles (NFTs).
  • This model is crucial for studying pre-NFT stages of AD, a window for potential therapeutic interventions.
  • A gap exists in molecular characterization of aged non-human primate (NHP) brains compared to human AD studies.

Purpose of the Study:

  • To perform spatially conserved molecular characterization in aged vervet brains, mirroring human AD analyses.
  • To identify regional and cell type-specific molecular changes associated with Aβ plaques in vervets.
  • To leverage advanced molecular techniques for understanding early AD mechanisms.

Main Methods:

  • Utilized fixed brain sections from 10 aged vervets (average 24.3 years) for neuropathological assessment.
  • Performed single-cell spatial transcriptomics on fresh-frozen parietal cortex using NanoString CosMx Spatial Molecular Imager and a human RNA 6K Discovery Panel.
  • Employed NanoString GeoMx Digital Spatial Profiler in a subset of vervets to analyze protein content around Aβ plaques.

Main Results:

  • Aβ plaques correlated with increased levels of Aβ-42, IBA1, GFAP, APP, and autophagy-related proteins.
  • Neurons adjacent to plaques displayed differential protein expression compared to distant neurons.
  • Spatial transcriptomics successfully annotated cell types (neurons, microglia, astrocytes, oligodendrocytes, endothelial cells) and mapped their distribution in the vervet parietal cortex.

Conclusions:

  • The vervet model offers a valuable platform for studying early AD molecular mechanisms due to the scarcity of human early AD data.
  • Molecular profiling in vervets identified cell type-specific changes driven by Aβ plaques.
  • These findings highlight potential novel therapeutic targets for early-stage Alzheimer's disease.