DNA β-Amyloid1-42 Trimer Immunization for Alzheimer Disease in a Wild-Type Mouse Model

Abstract

Alzheimer disease (AD) is the most common cause of age-related dementia characterized by memory loss and cognitive decline. The pathogenesis of AD has been associated with the accumulation, aggregation, and deposition of β-amyloid (Aβ) peptides in the brain. Amyloid plaques and neurofibrillary tangles are both hallmarks of AD. The amyloid cascade hypothesis was formulated 15 years ago, postulating Aβ deposition as the initial event in the multifactorial pathogenesis of AD.^1-3 In triple-transgenic AD mouse models, it has been shown that Aβ assembly precedes tau pathology.^4,5