Triggering Body's Natural Cell Recycling Process Could Treat Alzheimers Disease
In cell biology, autophagy, or autophagocytosis, is a process that involves the degradation and recycling of a cell’s own components. It is a tightly regulated process that plays a normal part in cell growth and development. Failure of autophagy is thought to be a main reason for the accumulation of cells responsible for damage and aging.
Low Calorie Diet May Prevent Neuron Damage by Triggering Autophagy Process
Because dementia in Alzheimer’s disease is in part caused by an aggregation of amyloid peptide into plaques, a team of scientists from Rockefeller University are investigating autophagy as a possible treatment to reduce or eliminate the built-up proteins and hopefully restore communication between neurons.
Most prior strategies for developing a drug to cure Alzheimer’s disease have focused on inhibiting the formation of amyloid-beta.
A team of researchers led by Yuan Tian, a postdoctoral fellow at Rockefeller, tested several compounds on rat and mice cells for their ability to reduce the buildup of amyloid-beta and found that SMER28 was the most effective. The team also compared the effect of SMER28 on amyloid-beta formation using normal cells and found three important autophagic players, one of them essential for SMER28’s effects.
The findings may also be beneficial for targeting twisted fibers of tau protein, another key element of Alzheimer’s disease. The mechanism could possibly be used to eliminate protein accumulation in other diseases as well, including Down syndrome, Huntington’s and Parkinson’s.
“By increasing our understanding of autophagy,” says Marc Flajolet, a research assistant professor, “it might be possible to stimulate it, pharmacologically or naturally, to improve the quality of life for aging people.”
Diet is one natural strategy suggested to prevent neuron damage. A low calorie diet might lead to higher autophagy activity that might delay or prevent aging and neurodegenerative diseases, says Flajolet. During nutrient starvation, increased levels of autophagy lead to the breakdown of non-vital components, ensuring that the vital processes can continue.
“Much effort has been carried out to prevent the formation of amyloid-beta without much success,” says Paul Greengard, head of the Laboratory of Molecular and Cellular Neuroscience. “In order to develop better-suited therapies, alternative approaches are clearly needed. One approach would be the identification of potential therapeutic targets that enhance the removal of amyloid-beta, for example, by increasing autophagy.”