Read here in full “Ziarul de Sănătate” no. 20
In a study published in the journal Cell Reports Medicine, American researchers explain how beta-amyloid deposits, which have been known for a long time, are present in the brains of Alzheimer’s patients as a kind of scaffolding for the accumulation of other proteins. .
Since many of these proteins are known to have signaling functions, their presence around amyloid aggregates, called plaques, could be to blame for damage to brain cells, more than amyloid itself, as current theories suggest. explains.
In the brains of people with Alzheimer’s, amyloid builds up and turns into sticky plaques that disrupt brain functions and cause cognitive decline.
The big unknown is still exactly how this will happen.
According to the most widely accepted hypothesis, beta-amyloid accumulation disrupts cell-to-cell communication and activates immune cells in a process that ultimately destroys brain cells.
In the recent study, Todd E. Golde, director of the Emory Center for Neurodegenerative Diseases at the Goizueta Institute, and Yona Levites, an associate professor at the Emory University School of Medicine, and their colleagues provide an opinion- a new hypothesis, emphasizing a different role for beta – amyloid, a simple protein that is present in the human brain but which usually spreads through natural processes.
In the experiments, Emory’s lab used cutting-edge analytical technologies to identify and measure levels of more than 8,000 proteins in human Alzheimer’s brains, as well as similar proteins in mice.
Focusing on the proteins whose levels were significantly increased, the researchers identified more than 20 proteins that accumulate with beta-amyloid in human and mouse Alzheimer’s brains.
As research continues, researchers suspect they will find more.
“As soon as we identified these new proteins, we wanted to know if they were just markers of Alzheimer’s disease or if they could change the fatal pathology of the disease,” explained Todd E. Golde.
What the research team at the Emory lab says
“To answer this question, we focused on two proteins, midkina and pleiotrophin. Our research showed that they accelerated amyloid accumulation both in the test tube and in mice. In other words, these extra proteins may play an important role in the process that leads to brain damage, rather than the amyloid itself. This suggests that they could form the basis of new treatments for this devastating neurological condition that has been very resistant to treatment over the years,” said the researchers.
Although the basics of Alzheimer’s disease have been understood for more than a century, the search for a cure has been slow, often marked by repeated rounds of initially promising treatments that failed in trials, as well as ongoing controversy. about competing theories that explain the best. the disease affects the brain.
According to the researchers, “the original theory of a purely linear amyloid cascade is now recognized as simplistic. Studies have shown the complexity of changes that occur over decades in the brain of individuals as Alzheimer’s pathologies appear.”
In particular, several types of amyloid aggregates other than beta-amyloid have been implicated in more than 30 human conditions that affect tissues and organs throughout the body.
Because this new research suggests a new process by which Alzheimer’s develops, it could enable new approaches to find treatment targets for other diseases as well.
Advertising and other video recommendations
2024-08-21 00:00:00
#discoveries #Alzheimers #disease #affect #brain
