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A protein fragment called amyloid-beta (Aβ) is known to aggregate and create plaque in the brains of Alzheimer's patients. Plaque hinders neuronal activity by gumming up synapses (spaces between cells through which chemical or electrical information is transmitted), eventually damaging nerve cell branches and leading to neuronal death.
In the current study, a collaborative team of researchers at the Gladstone Institute and the Baylor College of Medicine in Houston, created a strain of mice that overproduces a precursor of Aβ known as amyloid precursor protein. Five to six months after birth, as plaque built up, these animals showed learning and memory deficits illustrated by their difficulty navigating mazes. During autopsies, researchers observed that rewiring had occurred in the late subjects' brains.