Certain types of “superspreader” protein clumps could play a key role in the proliferation of Alzheimer’s disease, according to a recent study published in the journal Science Advances.
The clumps, known as fibrils, spread rapidly which cause other proteins to form toxic clusters that damage brain cells, the researchers noted in an Oct. 28 study published in the academic journal.
As part of the study, researchers watched these fibrils in action using advanced imaging. Based on their research, they believe that understanding how these clumps spread might lead to a better understanding of Alzheimer’s disease, leading to more effective treatments or early diagnostic tools.
The formation of the “potentially toxic molecules” on the surface of these protein clumps was studied from early to late stages over a period of hours, according to an article published by Swiss Federal Laboratories for Materials Science and Technology (EMPA).
The diagnosis and treatment of Alzheimer’s disease and other cognitive diseases remain “one of the greatest challenges facing modern medicine,” the article continues.
The reason the protein clumps were termed “superspreaders” was the nanometer-thin fibrils “ensure the spread of the disease” in brain tissue. Researchers were able to follow the process of fibril formation in real time, from the first moment to exceeding 250 hours.
Observations were compared and included in molecular model calculations, which allowed for researchers to categorize the protein clumps as being “superspreader” fibrils.
“This work brings us another step closer to better understanding how these proteins spread in brain tissue of Alzheimer’s disease ,” says EMPA researcher Peter Nirmalraj, who led the study along with collaboration from Irish University of Limerick.
Nirmalraj told EMPA in the article he hopes this could lead to new ways of monitoring Alzheimer’s disease progress and help inform future diagnostic tools.
The research was funded by Dementia Research Switzerland Synapsis Foundation.