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Unstable genetic elements in mitochondria may become ‘uncaged’ in Alzheimer’s disease
With researchers floundering in Alzheimer’s research as many promising drugs continue to fail, some are forming new theories about what might drive the disease. One of these revolves around dysfunctional mitochondria. A new hypothesis Researchers at Duke University have formed a new hypothesis called the ‘Alu Neurodegeneration Hypothesis’, which proposes that control over short, jumping genetic elements called Alus is loosened during aging; leaving them to wreak havoc on mitochondria and drive Alzheimer’s disease.“Alu elements are a double-edged sword. Once dismissed as selfish or junk DNA, they are now recognized as contributors to the diversity and complexity of the human brain. “They can provide new and beneficial gene functions. They have helped humans evolve higher cognitive function, but perhaps at the cost of neuron vulnerability that increases with age”
3-D modeling of the TOMM40 gene Credit: Peter Larsen
“We need to start thinking outside of the box when it comes to treating neurological diseases like Alzheimer’s”
While at this point the theory is far from proven, it raises some new interesting questions and may represent a new drug target too. It’s looking increasingly likely that Alzheimer’s is a complex disease with multiple contributing factors, so placing all our eggs in one basket may be a foolish approach. Attempting to deal with microbial burden, inflammation, mitochondrial dysfunction and microglial rejuvenation all at once for example could be something to watch for in the future. The importance of treating the disease early has also been underlined recently, so it may be that medical approaches applied in early stage and late stage Alzheimer’s patients may have very different effects. Read more at MedicalXpressCopyright © Gowing Life Limited, 2025 • All rights reserved • Registered in England & Wales No. 11774353 • Registered office: Ivy Business Centre, Crown Street, Manchester, M35 9BG.