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Updated: May 17, 2025
Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
Mouse models of Anti-Aβ immunotherapies
Philip Pikus1,2, R Scott Turner3, G William Rebeck4
1Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Rd, NW, District of Columbia, Washington, 20007, USA.
Background:
The development of anti-amyloid-beta (Aβ) immunotherapies as the first disease modifying therapy for Alzheimer's Disease (AD) is a breakthrough of basic research and translational science.
Main Text:
Genetically modified mouse models developed to study AD neuropathology and physiology were used for the discovery of Aβ immunotherapies and helped ultimately propel therapies to FDA approval. Nonetheless, the combination of modest efficacy and significant rates of an adverse side effect (amyloid related imaging abnormalities, ARIA), has prompted reverse translational research in these same mouse models to better understand the mechanism of the therapies.
Conclusion:
This review considers the use of these mouse models in understanding the mechanisms of Aβ clearance, cerebral amyloid angiopathy (CAA), blood brain barrier breakdown, neuroinflammation, and neuronal dysfunction in response to Aβ immunotherapy.
