A group of scientists from the U.S., U.K., and Portugal have potentially discovered a means of correcting the root protein mechanism that triggers dementia. They posited that stress could degrade cellular function to the point of hampering protein synthesis and proper “folding.” When misfolded proteins accumulate, the resulting aggregates might negatively affect neuron function.
Testing this hypothesis entailed stressing the endoplasmic reticulum (ER), a membrane structure within cells that produces slightly less than a third of the body’s proteins. In what constitutes a stunning outcome, the ER corrected the folding issue when under certain duress. “We were astonished to find that stressing the cell actually eliminated the aggregates – not by degrading them or clearing them out, but by unraveling the aggregates, potentially allowing them to refold correctly,” said Edward Avezov, a Group Leader at the University of Cambridge’s UK Dementia Research Institute.
This result goes against previous research – ultimately deemed inconclusive – that found ER stress to be a contributing factor in the development of Alzheimer’s disease. In the new study, cells from a hamster, mouse, and monkey were tested with ER stress induced by a calcium or carbohydrate inhibitor. Rapid light patterns were used to visualize protein folding.
Avezov cautions that despite the findings holding massive potential for new therapeutic vectors in averting Alzheimer’s development, stimulating stress in cells could still leave them in an overall worse state.
