Stress May Hasten Progression of Alzheimer’s Disease

September 18, 2006

September 18, 2006

Studies suggest that stress may play an important role in the progression of Alzheimer’s, a disease that causes damage to parts of the brain essential for thinking and memory. Scientists at the University of California at Irvine found that mice injected with a drug that mimics stress in people had high levels of beta-amyloid, a toxic protein that builds up in the brains of those with Alzheimer’s disease. The findings suggest that managing stress and avoiding certain medications that trigger stress hormones may be important parts of an Alzheimer’s care plan.

The mice had been genetically modified to develop a brain ailment that resembles Alzheimer’s in people. When young animals were given injections of dexamethasone, a substance similar to stress hormones in people, levels of toxic beta-amyloid jumped by 60 percent. Buildup of beta-amyloid is tied to the formation of brain-damaging plaques in the brain, a hallmark of Alzheimer’s disease. The researchers also found that levels of another protein called tau also increased in the mice. Tau is linked to so-called tangles in the brain, another characteristic of Alzheimer’s. The findings appeared in the Journal of Neuroscience.

“It is remarkable that these stress hormones can have such a significant effect in such a short period of time,” said study leader 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 development of brain defects was hastened in young animals, as well as in older mice that already had some buildup of plaques and tangles. The increased accumulation of beta-amyloid and tau also appeared to work in a “feedback loop” to hasten the progression of Alzheimer’s, the researchers note. They found that higher levels of beta-amyloid and tau led to an increase in the levels of the stress hormones, which would speed up the formation of more plaques and tangles.

Although it’s a long way from mice to people and much more research needs to be done, the investigators believe that these findings may have important implications for people with 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 behavior and co-author of the paper. “Some medications prescribed for the elderly for various conditions contain glucocorticoids.”  Green speculates that these drugs may be leading to accelerated cognitive decline in patients in the early stages of Alzheimer’s.  However, it is not known whether these drugs will have the same effect in humans.

Stress is a natural response as memory fades and everyday tasks become more difficult during the early stages of Alzheimer’s disease. This study suggests that managing that stress may be important for helping to slow the downward spiral of disease progression. We at the Fisher Center strongly agree with the idea that stress reduction is critically important in caring for the person with Alzheimer’s disease. Other research has shown that counseling and care from a team of experienced health-care providers may be key to managing stress, both in those with Alzheimer’s and those who care for them. Also, talk to your doctor about the medications you take.

www.Alzinfo.org, the Alzheimer’s Information Site, offers a wealth of expert advice on Alzheimer’s and caring for a loved one with the disease. For information on family support, therapeutic activities, and the care of Alzheimer’s disease, visit the alzinfo.org discussion on Continuing Care.

By www.ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.


Journal of Neuroscience, August 30, 2006. University of California, Irvine.


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