While previous studies have already revealed that stress boosts the production of a brain peptide critical to Alzheimer's disease, a new study on mice has now shown that blocking a different brain peptide slows the stress-induced increases.
The study, reported online in the Proceedings of the National Academy of Sciences by scientists from Washington University School of Medicine in St. Louis, is among the first studies to elaborate the basic biomolecular mechanisms that may underlie the increased risk of Alzheimer's disease.
AdvertisementLast November, the researchers had shown that the raising of genetically modified mice under isolated conditions in smaller cages accelerated the deposition of brain plaques and declines in cognitive ability. Since brain plaques are mostly comprised of a peptide known as amyloid beta, the researchers suspected that stress was increasing its levels.
In the present study, the scientists used a technique known as micro dialysis to monitor amyloid beta levels in the brains of mice exposed to the same stressors—isolation and smaller cages.
"Stress remarkably elevated soluble amyloid beta levels in the spaces between brain cells," says senior author Dr. David Holtzman, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology.
"But we didn't know based on those initial experiments if it was a chronic effect or a much more immediate effect. If it was more immediate, we thought we might be able to identify some of the brain molecules involved in increasing the levels," he added.
Initially, the researchers suspected corticosterone molecules, the mouse equivalent of the human stress hormone cortisol, to be behind the rapid change in the levels of amyloid. But upon seeing that a large dose of corticosterone didn't cause a similar rapid change in amyloid beta levels, they began searching for molecules released in the mouse brain by stress.
The investigators identified corticotropin-releasing factor (CRF) that is linked to increased levels of brain cell communication, which that in turn has already been associated to increased amyloid beta by previous studies.
When they directly placed CRF in the mouse brain, amyloid beta levels rose immediately. However, when mice were given a CRF blocker, stressed animals did not display increased amyloid beta.
"There are very few known environmental risk factors for Alzheimer's disease. Head trauma increases risk, higher education lowers it. Stress may be another environmental factor that increases risk," Holtzman notes.
He believes that drugs that block CRF or reduce anxiety may provide a new way to decrease amyloid beta, and eventually delay or prevent Alzheimer's disease. The researchers are continuing to explore connections between brain cell activity and amyloid beta levels.
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