Previous studies have pinpointed the role of stress in Alzheimer”s disease and other neurodegenerative disorders.
Now, scientists at the USC have discovered why.
Corresponding author Kelvin J. A. Davies, the James E. Birren Chair at the USC Davis School of Gerontology, and Professor of Molecular and 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 overexpression 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.
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 overexpression 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.
The study has tremendous implications for understanding and treating Alzheimer”s disease, the authors say.
The study has been published in the Journal of the Federation of American Societies for Experimental Biology.