New findings out of Emory University are challenging existing theories about the origins of Alzheimer's, the leading cause of dementia in the elderly worldwide. A team led by researchers at the Goizueta Brain Health Institute has found strong evidence supporting a new understanding of the mechanism behind Alzheimer's disease. In a paper published August 9 in Cell Reports Medicine , Todd E.
Golde and Yona Levites explain how the amyloid beta deposits long known to build up in the brains of Alzheimer's patients serve as a kind of scaffold for the accumulation of other proteins. Because many of these proteins have known signaling functions, their presence around the amyloid accumulations, known as plaques, could be the culprit causing brain cell damage rather than the amyloid itself. In the brains of those who suffer from Alzheimer's, amyloids accumulate and build up into sticky plaque that disrupts brain functions and causes cognitive decline.
The big unknown has been exactly how that occurs. According to the most widely adopted hypothesis, the amyloid beta buildup disrupts cell-to-cell communication and activates immune cells in a process that eventually destroys brain cells. In the study, Golde, director of the Emory Center for Neurodegenerative Disease in the Goizueta Institute, Levites, associate professor in Emory University's School of Medicine, and their colleagues presented a new hypothesis, emphasizing a different role for amyloid beta, a simple protein that forms in a.