Text Size Normal Text Sizing Button Medium Text Sizing Button Large Text Sizing Button Text Contrast Normal Contrast Button Reverse Contrast ButtonSwitch to Spanish Language Press Room Contact Us Sitemap Sign In Register
Link to Homepage About BrightFocus
BrightFocus
Donate Now Get Involved  
Alzheimer's Disease Research Macular Degeneration Research National Glaucoma Research


Stay Informed: Medical and Research Updates
Connect With Us!
 

 

Scientists Uncover Mechanism By Which Chronic Stress Causes Brain Disease

June 29, 2011

Chronic stress has long been linked with neurodegeneration. Scientists at USC now think they may know why.

The study, which has tremendous implications for understanding and treating Alzheimer's disease, was published in the June issue of The FASEB Journal (the Journal of the Federation of American Societies for Experimental Biology).

Corresponding author Kelvin J. A. Davies, the James E. Birren Chair at the USC Davis School of Gerontology, and Professor of Molecular & Computational Biology in the USC Dornsife College, examined the brains of rats that had experienced psychological stresses and found high levels of the RCAN1 gene. Davies and his colleagues suggest that chronic stress—physical or mental—causes over-expression of RCAN1, in turn leading to neurodegenerative disease.

Think of a gene as a pattern or mold that generates specific proteins. For example, if 200 RCAN1 proteins are built where only 100 were needed, scientists would describe this as "overexpression" of the RCAN1 gene.

In a healthy person, the RCAN1 gene helps cells cope with stress. Overproduction, however, can eventually damage neurons, preventing the brain's signals from traveling and causing disease.

Chronic overproduction of RCAN1 causes hyper-phosphorylation of tau proteins in the brain.

Tau proteins stabilize microtubules, which are like the scaffolding used to build the brain's neurons. Previous research has shown that when the tau protein binds too much phosphate—a process called hyperphosphorylation—it forms snarls that prevent the brain's signals from effectively traveling.

"One can imagine that it becomes sticky and makes tangled scaffolding," Davies said.

These neurofibrillary tangles eventually choke the life out of neurons, killing off brain function a tiny piece at a time in what is outwardly recognized as degenerative brain disease.

Currently, there are two competing theories about the leading cause of neurodegeneration in Alzheimer's disease: overproduction of the Amyloid Beta peptide and tau hyperphosphorylation. Research in the Davies lab suggests that over-expression of RCAN1 is connected to both, and appears to unite the Amyloid Beta and tau theories of neurodegeneration.

"Both are clearly important, and RCAN1 could be the link," Davies said.

RCAN1 has been shown to be chronically over-expressed from birth in the brains of patients with Down syndrome. These patients develop neurofibrillary tangles and typically start to experience the onset of Alzheimer's disease around age 40.

Davies' lab has also shown a connection between too little RCAN1 production and Huntington's disease. "Our results suggest that the cellular levels of RCAN1 proteins must be kept within a fairly narrow range in order to avoid serious dysfunction," Davies said.

"By publishing this hypothesis, we hope to stimulate more research on the subject," he said.

Adapted from the University of Southern California

View all news updates for Alzheimer's disease


Disclaimer: The information provided in this section is a public service of the BrightFocus Foundation, and should not in any way substitute for the advice of a qualified healthcare professional, and is not intended to constitute medical advice. Although we take efforts to keep the medical information on our website updated, we cannot guarantee that the information on our website reflects the most up-to-date research. Please consult your physician for personalized medical advice; all medications and supplements should only be taken under medical supervision. BrightFocus Foundation does not endorse any medical product or therapy.

Some of the content in this section is adapted from other sources, which are clearly identified within each individual item of information.

Shop for a Cause YouTube Twitter Connect With Us Pinterest Google+