The latest round of failed drug trials for Alzheimer's has researchers questioning the reigning approach to battling the disease, which focuses on preventing a sticky protein called amyloid from building up in the brain. Duke University scientists have identified a mechanism in the molecular machinery of the cell that could help explain how neurons begin to falter in the initial stages of Alzheimer's, even before amyloid clumps appear. This rethinking of the Alzheimer's process centers on human genes critical for the healthy functioning of mitochondria, the energy factories of the cell, which are riddled with mobile chunks of DNA called Alu elements. If these "jumping genes" lose their normal controls as a person ages, they could start to wreak havoc on the machinery that supplies energy to brain cells -- leading to a loss of neurons and ultimately dementia, the researchers say. And if this "Alu Neurodegeneration Hypothesis" holds up, it could help identify people at risk sooner, before they develop symptoms, or point to new ways to delay onset or slow progression of the disease, said study co-author Peter Larsen, Ph.D., Senior Research Scientist in co-author Biology Professor Anne Yoder's lab at Duke. The researchers describe the Alu neurodegeneration hypothesis in a paper published online on March 8, 2017 in Alzheimer's & Dementia: The Journal of the Alzheimer's Association. The open-access article is titled “The Alu Neurodegeneration Hypothesis: A Primate-Specific Mechanism for Neuronal Transcription Noise, Mitochondrial Dysfunction, and Manifestation of Neurodegenerative Disease.” The dominant idea guiding Alzheimer's research for 25 years has been that the disease results from the abnormal buildup of hard, waxy amyloid plaques in the parts of the brain that control memory.
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