Khaberni - A research team from the University of California, Santa Cruz, has revealed that decades of studies on dementia have focused on the wrong protein.
Instead of focusing on amyloid beta, the known protein for forming clumps in the brain that disrupt communication between neurons, the team points to another protein called P3 or amyloid alpha, which was previously thought to be harmless.
According to the study, P3 protein is produced at the same time with amyloid beta from the amyloid precursor protein (APP) by the enzymes beta-secretase and gamma-secretase, but it is considered a byproduct. It may be toxic to neurons and form the same harmful clumps that cause brain damage.
The researchers reviewed many previous studies and conducted 3 of their own studies that showed P3 might be more capable of forming harmful protein deposits and possibly faster than amyloid beta.
Dr. Yevgeny Raskatov, the chemist who led the study, said: "P3 is likely not as innocent as previously thought. These findings could completely change the course of Alzheimer's research."
He added: "P3 is a peptide that aggregates distinctly and could be toxic to nerves and contribute to the progression of the disease."
Dr. David Teplow, a distinguished professor of neuroscience at the University of California, Los Angeles, after reviewing the team's work, mentioned that the results "change our understanding of the disease and have significant implications on fundamental science and clinical research for its treatment."
The team affirmed that the results open the door for the development of new treatment methods that target P3 protein, highlighting the need for more research to fully understand its role in Alzheimer's disease.
