Anti-pyroglutamate-3 Aβ immunotherapy engages microglia and inhibits amyloid accumulation in transgenic mouse models of Aβ amyloidosis

Liao F
Abbvie
June 2, 2025
Acta Neuropathol
https://pubmed.ncbi.nlm.nih.gov/40455292

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/40455292

Research summary

This study evaluates a monoclonal antibody targeting pyroglutamate-modified Aβ (pGlu3-Aβ), demonstrating reduced amyloid plaque load, enhanced microglial engagement, and preserved synaptic integrity in Alzheimer’s disease models.

Key outcome of the study

pGlu3-Aβ immunotherapy reduces plaque load, activates microglia, and protects synapses, suggesting therapeutic potential in AD.

Model

Transgenic hAPP mouse crossed with genOway’s Cx3cr1-CreERT2-tdTomato line for microglial lineage tracing and activation analysis.

TARGET:
APP, Cx3cr1
Amyloid beta precursor protein, CX3C chemokine receptor 1

Keywords

Alzheimer’s disease, Neuroinflammation, Microglial activation, Immunotherapy

Technical specifications

Humanized APP model, Inducible CreERT2, tdTomato reporter, Microglial tracing, Knockin at endogenous Cx3cr1 locus

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Reporter KI mouse

Use a reporter mouse Knockin for in vivo monitoring of transcriptional promoter activity, protein localization, cell trafficking, etc.