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.
ABCA7 modulates neuroinflammation in AD by regulating NLRP3 inflammasome activation in microglia and astrocytes; its deficiency exacerbates Aβ pathology and inflammatory responses.
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.
Alzheimer's disease, Neuroinflammation, ABCA7, NLRP3 inflammasome, Microglia, Astrocytes
Humanized Knockin model, Cre-inducible ABCA7^flx, APPPS1-21 crossbreeding, Neuroinflammatory pathway analysis
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
