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,…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 Peter Larsen, senior research scientist at Duke.
Larsen used 3D modeling to show that Alu insertions within the TOMM40 gene could…[cause] the mitochondria’s import machinery to clog and stop working.
The TOMM40 gene is one example, the researchers say, but if Alus disrupt other mitochondrial genes, the same basic mechanism could help explain the initial stages of other neurodegenerative diseases too, including Parkinson’s disease, Huntington’s disease and amyotrophic lateral sclerosis (ALS).
[The study can be found here.]
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