SEP 21, 2015 02:14 PM PDT

Stress Hormone and Alzheimer's

Is there a connection between the brain’s stress response and a protein related to Alzheimer’s disease? Researchers at the University of Florida think so, as related in an article published in Futurity
Study says stress-coping hormone triggers amyloid beta, which leads to Alzheimer's disease. 
A new study – funded by the National Institutes of Health and the US Department of Veterans Affairs -- with a mouse model and human cells demonstrates that a stress-coping hormone released by the brain boosts the production of protein fragments called amyloid beta. These fragments trigger the brain degeneration that leads to Alzheimer’s disease. The results shed light on the possible relationship between stress and Alzheimer’s disease, which is believed to stem from a mix of genetic, lifestyle and environmental factors. The findings strengthen the idea of a connection between stress and Alzheimer’s disease.
 
According to Todd Golde, professor of neuroscience at the University of Florida, “It adds detailed insight into the stress mechanisms that might promote at least one of the Alzheimer’s pathologies.”
 
It is especially challenging to determine the non-genetic factors that heighten the risk of Alzheimer’s disease. The study helps to look at the effects of stress and other environmental factors and offers guidance for new treatment approaches in the future.
 
Stress triggers the release of the hormone corticotrophin releasing factor, or CRF, in the brain, and that increases production of amyloid beta. When amyloid beta collects in the brain, it starts a complex degenerative cascade that leads to Alzheimer’s disease.
 
In the new study mice exposed to acute stress had more of the Alzheimer’s-related protein in their brains than mice in a control group. Additionally, the stressed mice had more of a specific kind of amyloid beta, one that has a particularly significant role in the development of Alzheimer’s disease, according to a report in the EMBO Journal. For a greater understanding of how CRF increases the amount of Alzheimer’s-related proteins, the researchers treated human neurons with CRF, triggering a considerable increase in the amyloid proteins involved in Alzheimer’s disease.
 
The experiments show more about the mechanics of a likely relationship between stress and Alzheimer’s disease. CRF causes the enzyme gamma secretase to increase its activity, which causes more of the Alzheimer’s-related protein to be produced, according to Golde.
 
Researchers believe that modifying environmental factors such as stress is an easier approach to warding off Alzheimer’s disease than modifying the genes that cause the disorder. Because blocking the CRF receptor that initiates the stress-induced process that generates Alzheimer’s-related proteins did not work, the researchers are contemplating an antibody that may be used to block the stress hormone directly.
 
Golde summarized, “These softer, non-genetic factors that may confer risk of Alzheimer’s disease are much harder to address, but we need more novel approaches in the pipeline than we have now.”
About the Author
  • Ilene Schneider is the owner of Schneider the Writer, a firm that provides communications for health care, high technology and service enterprises. Her specialties include public relations, media relations, advertising, journalistic writing, editing, grant writing and corporate creativity consulting services. Prior to starting her own business in 1985, Ilene was editor of the Cleveland edition of TV Guide, associate editor of School Product News (Penton Publishing) and senior public relations representative at Beckman Instruments, Inc. She was profiled in a book, How to Open and Operate a Home-Based Writing Business and listed in Who's Who of American Women, Who's Who in Advertising and Who's Who in Media and Communications. She was the recipient of the Women in Communications, Inc. Clarion Award in advertising. A graduate of the University of Pennsylvania, Ilene and her family have lived in Irvine, California, since 1978.
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