Abi3 S212F Alzheimer's disease variant alters plaque structure and disrupts microglia

Key Points

To understand how the Abi3 S212F variant impacts amyloid pathology and microglial behavior in vivo.
Developed a mouse model carrying the Abi3 S212F variant and crossed it with humanized amyloid beta models.
Analyzed amyloid pathology, microglial dynamics, and remodeling using confocal imaging and spatial transcriptomics across the mouse lifespan.
Performed biochemical assays and single-cell analyses to explore microglial states.
The Abi3 S212F variant led to reduced dense-core plaque compaction, lowering dense-core burden without affecting diffuse Aβ levels.
Microglial loss occurred via apoptosis and pyroptosis, highlighting a vulnerability that was evident even without plaque presence.
Spatial transcriptomics indicated an age-dependent shift in microglial states toward Abi3-high, predisposing them to degeneration.

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Reveals altered plaque structure and microglial dysfunction in a mouse model, indicating new therapeutic targets.

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Butler et al. (2026) studied this question.

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