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Alzheimer's, Dementia & Mental Health
Stress Significantly and Quickly Hastens the
Progress of Alzheimer's Disease
Stress hormones play central role in AD
development, progression
 August 30, 2006 - Stress hormones appear to rapidly
exacerbate 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 and reducing certain medications prescribed
for the elderly could slow down the progression of this devastating
disease.
In a study with genetically modified mice, Frank
LaFerla, professor of neurobiology and behavior, and a team of UCI
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.
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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 findings appear in this week’s issue of the Journal of Neuroscience.
“It is remarkable that these stress hormones can
have such a significant effect in such a short period of time,” LaFerla
said.
“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.
“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 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.”
Alzheimer’s disease is a progressive
neurodegenerative disorder that affects 4.5 million to 5 million adults
in the United States. If no effective therapies are developed, it is
estimated that 13 million Americans will be afflicted with the disease
by 2050.
In recent years, LaFerla has been at the forefront
of Alzheimer’s research. He and other members of his research team
developed the transgenic mice used in this study, which are now a model
for studying Alzheimer’s around the world. Earlier this year, he
announced work on a new compound that not only relieves the cognitive
symptoms of Alzheimer’s disease, but also reduces the plaques and
tangles in the brain.
Lauren Billings, postdoctoral researcher, and Benno
Roozendaal, assistant researcher in neurobiology and behavior,
collaborated on the study. The work was funded by grants from the
Alzheimer’s Association, the National Institutes of Health and the
National Institute of Mental Health.
About the University of California, Irvine: The
University of California, Irvine is a top-ranked university dedicated to
research, scholarship and community service. Founded in 1965, UCI is
among the fastest-growing University of California campuses, with more
than 24,000 undergraduate and graduate students and about 1,400 faculty
members. The second-largest employer in dynamic Orange County, UCI
contributes an annual economic impact of $3.3 billion. For more UCI
news, visit
www.today.uci.edu.
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