Animal models of Alzheimer's disease with rapid onset of amyloid-beta plaque lesions
By using compositions with APP and PSEN1 mutations and neuron-specific promoters, the method accelerates AD phenotypes in non-human animals, addressing the limitations of existing models and facilitating rapid evaluation of therapeutic agents.
JP2026519491APending Publication Date: 2026-06-16REGENERON PHARMACEUTICALS INC
Patent Information
- Authority / Receiving Office
- JP · JP
- Patent Type
- Applications
- Current Assignee / Owner
- REGENERON PHARMACEUTICALS INC
- Filing Date
- 2024-06-07
- Publication Date
- 2026-06-16
AI Technical Summary
Technical Problem
Existing transgenic mouse models for Alzheimer's disease (AD) are time-consuming and do not exhibit lesions for extended periods, with most lesions appearing only after 6 months of age, necessitating the development of more efficient and rapid models.
Method used
Compositions comprising nucleic acids encoding amyloid-beta precursor protein (APP) and presenilin-1 (PSEN1) are used to create non-human animal models, with specific mutations and promoters to accelerate the onset of AD phenotypes, such as Aβ plaque lesions, within one to two months.
Benefits of technology
The proposed method enables the rapid development of AD models in non-human animals, allowing for efficient evaluation of therapeutic agents and providing insights into AD progression and treatment strategies.
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Smart Images
Figure 2026519491000001_ABST
Abstract
This specification provides for compositions comprising nucleic acids encoding amyloid-beta precursor protein and / or nucleic acids encoding presenilin-1, cells comprising the compositions, animals comprising the compositions, methods for producing cells and animals, methods for modeling Alzheimer's disease, methods for evaluating candidate therapeutic agents for the treatment of Alzheimer's disease or improvement of symptoms or phenotypes of Alzheimer's disease, and methods for evaluating candidate therapeutic agents for the prevention of Alzheimer's disease or prevention of symptoms or phenotypes of Alzheimer's disease.
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