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Basic Science and Pathogenesis.

Matthew Mandrozos1,2, Tina Beckett2, Mary Hill2

  • 1University of Toronto, Toronto, ON, Canada.

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Summary
This summary is machine-generated.

This study developed a novel rat model for Lewy Body Variant of Alzheimer's disease (LBV-AD) by injecting alpha-synuclein into the brain. The model successfully replicated key LBV-AD pathologies, showing increased alpha-synuclein aggregates over time.

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Area of Science:

  • Neuroscience
  • Pathology
  • Animal Models

Background:

  • Alzheimer's disease (AD) is marked by amyloid-beta and tau pathology.
  • Co-pathologies, like Lewy Bodies (LBs) common in Parkinson's disease, contribute to AD heterogeneity.
  • Lewy Body Variant of AD (LBV-AD) shows accelerated progression.

Purpose of the Study:

  • To characterize a novel preclinical rat model for LBV-AD.
  • To recapitulate the main pathological hallmarks of LBV-AD in a preclinical setting.

Main Methods:

  • Stereotaxic injection of adeno-associated virus (AAV) carrying human alpha-synuclein (hSNCA or SYN119) into F344TgAD and non-transgenic rats.
  • Analysis at 3, 5, and 9 months post-injection, including histology to quantify pathology and neurodegeneration markers.

Main Results:

  • Alpha-synuclein aggregates were observed in the amygdala and striatum by 3 months post-injection.
  • A trend of increased aggregates was noted in transgenic rats initially.
  • Significantly more Lewy Body pathology was found in non-transgenic rats injected with hSNCA at 5 months.

Conclusions:

  • Both hSNCA and SYN119 successfully produced alpha-synuclein aggregates in the rat brain.
  • Aggregate levels increased over time, supporting the model's utility for studying LBV-AD progression.