A newly discovered mechanism that is activated when cells become “stressed” may open a pathway to help prevent the protein aggregation commonly seen in cells. neurodegenerative diseases As the Alzheimer’s and the Parkinson’s.
In the research led by the University of Cambridge (United Kingdom), which publishes Nature Communications, it is explained that a characteristic of diseases such as Alzheimer’s and the Parkinson’s is the accumulation of misfolded proteins that form aggregates with the ability to cause irreversible damage to neurons.
Protein folding is a normal process in the body and, in healthy individuals, cells have a kind of quality control to ensure that those that do poorly are destroyed, but in the neurodegenerative diseasesthis system deteriorates, with potentially devastating consequences.
The newly identified mechanism appears to reverse accumulation of aggregatesbut not completely removing them, but rather folding them back.
“Just as when we get stressed by a heavy workload, cells can also become ‘stressed’ if they are asked to produce a large amount of protein”for example when they produce antibodies in response to an infection, explained Edward Avezov of the University of Cambridge.
The team focused on stress a component of cells called the endoplasmic reticulum. The initial hypothesis was that stressing the endoplasmic reticulum could lead to misfolding and aggregation of proteins by decreasing their ability to function properly, but the result they discovered was just the opposite.
By stressing the cell, the aggregates were removed, not because they degraded, but because they unraveled, allowing them to refold properly.
“If we can find a way to wake up this mechanism without stressing cells – which could do more harm than good – then we might find a way to treat some dementias.”Avezov said.
The main component of this mechanism appears to be a class of proteins known as heat shock (HSP)which are made in greater quantity when exposed to temperatures above their normal growth temperature, and in response to stress.