
This episode discusses the historical context and implications of amyloid plaques in Alzheimer's Disease and the development of animal models for research.
Last week we reviewed two seminal studies from the 1990s, both showing mathematically that amyloid plaques are, at best, an inconsistent bystander in Alzheimer’s Disease. Plainly, they are not the driving cause. Hardcore believers may have ignored or rationalized the findings from these small but pivotal autopsy studies. A decade later however, there would be no refuge and no rescue when two trials shook the neurology community, forcing even the most avid and invested supporters to abandon ship. Of Mice To test dementia treatments, researchers needed test subjects. In the early ‘90s geneticists made a game-changing discovery : A tiny fraction of people (roughly 1%) possess a rare genetic mutation directly linked to amyloid processing. Star-crossed and dementia-bound, those who carry the mutation typically develop early-onset Alzheimer’s and massive amounts of amyloid plaque. In 1996, researchers at the University of Minnesota famously spliced these defective genes into a mouse, creating the Tg2576 animal model—a transgenic mouse with early cognitive decline and heavy accumulations of amyloid. Recognizing the goldmine this could represent to a pharmaceutical industry that had for…
Host: David Newman
Organizations: University of Minnesota, pharmaceutical industry, Tg2576
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