A new study conducted by Emory University is helping overturn the traditional theories about the origins of Alzheimer’s disease, globally the leading cause of dementia. Researchers at the Goizueta Brain Health Institute at Emory University have come up with compelling evidence to point out a different mechanism behind the disease, thereby opening a new avenue for the treatment of life thinners.
In a paper published in Cell Reports Medicine, Todd E. Golde of the University of Florida and Yona Levites provide details on how, rather than being direct actors, amyloid beta deposits may end up acting as scaffolds for other proteins that cause brain cell damage, a possibly groundbreaking concept. These proteins seem to accumulate around the amyloid plaques and could be agents of harm with known signaling functions.
For decades, the working hypothesis has been that the accumulation of amyloid beta disrupts intercellular communication and activates immune cells, which then destroy brain cells. However, by showing this new role of amyloid beta, Golde, director of the Emory Center for Neurodegenerative Disease, and Levites, an associate professor at Emory University’s School of Medicine, may point to a possibility that this protein is not directly responsible for the noesis.
These researchers used state-of-the-art analytical technologies to identify and measure more than 8,000 proteins in human brains affected by Alzheimer’s, as well as in mice. They identified over 20 proteins that co-accumulate with amyloid beta in the human and mouse brain. Golde explains, “Once we identified these new proteins, we wanted to know whether they were merely markers of Alzheimer’s or if they could alter the disease’s deadly pathology.”
Working on two proteins, the researchers found that midkine and pleiotrophin accelerated the aggregation of amyloids in test tubes and mice. That implies these other proteins might have a principal role in the process of brain damage, providing new targets for therapies. “This suggests they might be a basis for new therapies for this terrible brain affliction that’s been frustratingly resistant to treatment over the years,” Golde notes.
While the basics of Alzheimer’s have been long known, a cure has turned out to be painfully slow and is beleaguered by reverses. The researchers now accept that their early ideas of a purely linear amyloid cascade are far too simplistic. Decades-long changes in the brains of people experiencing the emergence of Alzheimer’s pathologies are incredibly complex, as studies now reveal.
Significantly, other forms of amyloid accumulation, apart from amyloid beta, have been implicated in over 30 human diseases affecting tissues and organs of the body. The new study suggests a mechanism for the development of Alzheimer’s that may potentially open up new avenues for finding treatment targets for other diseases as well.
This newly found mechanism of the disease can become a turning point in searching for an effective treatment for Alzheimer’s. An extremely important point of this study, it had highlighted that by searching beyond amyloid beta, one could get a hold of the complexities of the Alzheimer’s mechanism of the disease to get more effective therapies.