This study investigates the role of EBP1 in modulating amyloid β (Aβ) pathology through regulation of γ-secretase. Loss of EBP1 increases Aβ production and deposition, while its restoration ameliorates cognitive impairments and reduces amyloid burden.
EBP1 negatively regulates γ-secretase activity. Its loss leads to increased Aβ production, plaque accumulation, and cognitive decline. Restoring EBP1 improves amyloid clearance and behavioral outcomes.
Conditional EBP1 Knockout mouse model generated by genOway, targeting the Pa2g4 gene. The model includes a reporter gene coupled via IRES and allows for Cre-dependent inactivation of EBP1 in specific tissues.
Alzheimer's disease, Amyloid β, γ-secretase, Neurodegeneration, Cognitive function
Conditional Knockout mouse model, IRES-reporter, Cre-lox system, Forebrain-specific targeting, AAV delivery, Behavioral testing
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
