Cognitive Labs

  



Stress hormones appear to rapidly accelerate the formation of brain lesions that are the hallmarks of Alzheimer's disease, according to researchers at UC Irvine. The findings suggest that managing stress could slow down the progression of this devastating disease.

When young animals were injected for just seven days with dexamethasone, a substance similar to the body's stress hormones, the levels of the protein beta-amyloid in the brain increased by 60 percent. After beta-amyloid production increases the protein fragments aggregate and form plaques; scientists also found that the levels of another protein, tau, also increased.

"It is remarkable that these stress hormones can have such a significant effect in such a short period of time," said Dr. Frank LaFerla. "Although we have known for some time that higher levels of stress hormones are seen in individuals in the early stages of Alzheimer's, this is the first time we have seen how these hormones play such a direct role in exacerbating the underlying pathology of the disease."

The researchers injected four-month-old transgenic mice with levels of dexamethasone similar to the level of hormones that would be seen in humans under stress. At this young age, there would be little formation of plaques and tangles in the brains of the mice. After one week, the scientists found that the level of beta-amyloid in the brains of the animals compared to what is seen in the brains of untreated eight- to nine-month-old mice, demonstrating the profound consequence of glucocorticoid exposure. When dexamethasone was given to 13-month-old mice that already had some plaque and tangle pathology, the hormone again significantly worsened the plaque lesions in the brain and led to increased accumulation of the tau protein.

"Although we expected that this drug, which, like the stress hormone cortisol, activates glucocorticoid receptors, might have some effect on plaques and tangles, it was surprising to find that such large increases were induced in relatively young mice," said James L. McGaugh, research professor of neurobiology and behavior and co-author of the paper.

The increased accumulation of beta-amyloid and tau appears to work in a "feedback loop" to hasten the progression of Alzheimer's. The researchers found that the higher levels of beta-amyloid and tau led to an increase in the levels of the stress hormones, which would come back to the brain and speed up the formation of more plaques and tangles.

According to the researchers, these findings have profound implications for how to treat the elderly who suffer from Alzheimer's disease.

Abstract

// posted by neurofuture9:45 AM permanent link