In a study with genetically modified mice, Frank LaFerla, professor of neurobiology and behaviour, and a team of University of California, Irvine researchers found that when young animals were injected for just seven days with dexamethasone, a glucocorticoid similar to the body’s stress hormones, the levels of the protein beta-amyloid in the brain increased by 60 percent. When beta-amyloid production increases and these protein fragments aggregate, they form plaques, one of the two hallmark brain lesions of Alzheimer’s disease. The scientists also found that the levels of another protein, tau, also increased. Tau accumulation eventually leads to the formation of tangles, the other signature lesion of Alzheimer’s.
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. “This study suggests that not only is stress management an important factor in treating Alzheimer’s disease, but that physicians should pay close attention to the pharmaceutical products they prescribe for their elderly patients,” said Kim Green, a postdoctoral researcher in neurobiology and behaviour and first author of the paper. “Some medications prescribed for the elderly for various conditions contain glucocorticoids. These drugs may be leading to accelerated cognitive decline in patients in the early stages of Alzheimer’s.”
MEDICA.de; Source: University of California, Irvine