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August 29, 2026Discover Neuroscience0 citationsOpen Access

Alpha-Synuclein Fibrils Induce Neurodegeneration and Blood-Brain Barrier Breakdown in Mice

Intranigral injection of alpha-synuclein pre-formed fibrils leads to BBB compromise and bilateral dopaminergic neurodegeneration in A53T alpha-synuclein transgenic mice

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Authors

SGSoumitra GhoshHLHan LinSCSarah Chu

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Overview

Preclinical animal model reveals bilateral neurodegeneration and blood-brain barrier compromise in A53T mice, indicating strong central-peripheral immune interactions in Parkinson's disease.

Key Points

  • To establish an animal model of Parkinson's disease that replicates core neuropathological features by injecting human alpha-synuclein pre-formed fibrils into A53T transgenic mice.
  • Administered a unilateral injection of human alpha-synuclein pre-formed fibrils into the substantia nigra of mutant A53T alpha-synuclein overexpressing mice.
  • Tracked the spread of phosphorylated alpha-synuclein pathology, neuroinflammation, dopaminergic cell loss, and blood-brain barrier integrity over a 60-day period.
  • Induced bilateral phosphorylated alpha-synuclein (pS129) pathology within 60 days that propagated to the striatum, cerebral cortex, and midbrain.
  • Caused bilateral dopaminergic neurodegeneration, demonstrated by a 50% reduction in tyrosine hydroxylase intensity in the substantia nigra and a 40% reduction in the striatum.
  • Compromised blood-brain barrier integrity and stimulated T-cell infiltration that correlated directly with pS129 pathology and neuroinflammation.

Cite This Study

Ghosh et al. (2026) studied this question.

synapsesocial.com/papers/6a9298aa8e5d7d1fc0c1080dhttps://doi.org/10.1186/s13064-026-00286-1
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