(RxWiki News) Scientists have long linked chronic stress to brain degeneration. Now they may have identified the connection. These findings could ultimately aid in understanding and treating Alzheimer's disease.
Gene overexpression can lead to neurological degeneration, according to researchers from University of Southern California. Awareness of this process can shed light on conditions that affect memory and decision-making skills.
"Do yoga to lower stress levels."
Author Kelvin J. A. Davies, the James E. Birren Chair at the USC Davis School of Gerontology and professor of molecular and computational biology at the USC Dornsife College of Letters, Arts and Sciences, examined the brains of rats that had experienced psychological stresses and discovered high levels of the RCAN1 gene.
The finding suggests that chronic mental or physical stress causes overexpression of RCAN1, which leads to neurodegenerative disease.
The RCAN1 gene helps healthy people cope with stress. Overproduction can eventually damage neurons, preventing the brain’s signals from traveling, which can cause disease. Chronic overproduction of the gene leads to hyperphosphorylation (a biological pricess) of tau proteins in the brain.
Tau proteins stabilize microtubules, which help build the brain’s neurons. When the tau protein binds too much phosphate -- a process called hyperphosphorylation -- it forms snarls so that the brain’s signals cannot effectively travel. The tangles eventually kill the neurons, damaging brain function one small piece at a time through what is known as degenerative brain disease.
Current theories about the cause of neurodegeneration in Alzheimer’s disease include either of the overproduction of the Amyloid beta peptide or tau hyperphosphorylation. The new research suggests that overexpression of RCAN1 is connected to both.
The USC research team was aided by scientists from Monash University of Australia and the Institute of Nuclear Sciences in Serbia. The study was funded by the National Institutes of Health and the CHDI Foundation Inc.