Remodeling Alzheimer-amyloidosis models by seeding

Alzheimer's disease (AD) is among the most prevalent neurodegenerative diseases, with brain pathology defined by extracellular amyloid beta deposits and intracellular tau aggregates. To aid in research efforts to improve understanding of this disease, transgenic murine models have been developed that replicate aspects of AD pathology. Familial AD is associated with mutations in the amyloid precursor protein and in the presenilins (associated with amyloidosis); transgenic amyloid models feature one or more of these mutant genes. Recent advances in seeding methods provide a means to alter the morphology of resultant amyloid deposits and the age that pathology develops. In this review, we discuss the variety of factors that influence the seeding of amyloid beta pathology, including the source of seed, the time interval after seeding, the nature of the transgenic host, and the preparation of the seeding inoculum.

Automated summary

Alzheimer's disease is characterized by extracellular amyloid beta deposits and intracellular tau aggregates. Transgenic murine models have been developed to replicate aspects of AD pathology. Recent advances in seeding methods have provided ways to alter the morphology of amyloid deposits and the age at which pathology develops.