The ABC transporter A7 modulates neuroinflammation via NLRP3 inflammasome in Alzheimer’s disease mice

Irene Santos-García
University of Oslo
January 27, 2025
Alzheimers Res Ther
https://pubmed.ncbi.nlm.nih.gov/39871385

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

https://pubmed.ncbi.nlm.nih.gov/39871385

Research summary

This study investigates the role of ABCA7 in modulating neuroinflammation through the NLRP3 inflammasome pathway in Alzheimer's disease (AD). Utilizing a humanized, Cre-inducible ABCA7^flx Knockin mouse model developed by genOway, crossbred with the APPPS1-21 β-amyloidosis model, researchers observed that constitutive Knockout of Abca7 led to increased Aβ42 levels and heightened activation of microglia and astrocytes. These changes were associated with upregulation of NLRP3 inflammasome components and proinflammatory cytokines. Interestingly, microglia-specific ABCA7 Knockout restored Aβ42 levels and inflammatory markers to baseline, highlighting the critical role of ABCA7 in microglia-astrocyte communication and neuroinflammatory regulation in AD.

Key outcome of the study

ABCA7 modulates neuroinflammation in AD by regulating NLRP3 inflammasome activation in microglia and astrocytes; its deficiency exacerbates Aβ pathology and inflammatory responses.

Model

Humanized, Cre-inducible ABCA7^flx Knockin mouse model developed by genOway, crossbred with APPPS1-21 to study the impact of ABCA7 on neuroinflammation and amyloid pathology in AD.

TARGET:
ABCA7
ATP-binding cassette sub-family A member 7

Keywords

Alzheimer's disease, Neuroinflammation, ABCA7, NLRP3 inflammasome, Microglia, Astrocytes

Technical specifications

Humanized Knockin model, Cre-inducible ABCA7^flx, APPPS1-21 crossbreeding, Neuroinflammatory pathway analysis

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