|Stress Hormone Impacts Memory, Learning in Diabetic Rodents
Diabetes is known to impair the cognitive health of people, but
now scientists have identified one potential mechanism underlying
these learning and memory problems. A new National Institutes
of Health (NIH) study in diabetic rodents finds that increased
levels of a stress hormone produced by the adrenal gland disrupt
the healthy functioning of the hippocampus, the region of the brain
responsible for learning and short-term memory. Moreover, when
levels of the adrenal glucocorticoid hormone corticosterone (also
known as cortisol in humans) are returned to normal, the hippocampus
recovers its ability to build new cells and regains the "plasticity" needed
to compensate for injury and disease and
adjust to change.
The study appears in the Feb. 17, 2008, issue of Nature Neuroscience and
was conducted by the National Institute on Aging (NIA),
part of the NIH. NIA's Mark Mattson, Ph.D., and colleagues
in the Institute's Intramural Research Program performed
the study with Alexis M. Stranahan, a graduate student at Princeton
University in New Jersey.
"This research in animal models is intriguing, suggesting
the possibility of novel approaches in preventing and treating
cognitive impairment by maintaining normal levels of glucocorticoid," said
Richard J. Hodes, M.D., NIA director. "Further study will
provide a better understanding of the often complex interplay between
the nervous system, hormones and cognitive health."
Cortisol production is controlled by the hypothalamic-pituitary
axis (HPA), a hormone-producing system involving the hypothalamus
and pituitary gland in the brain and the adrenal gland located
near the kidney. People with poorly controlled diabetes often
have an overactive HPA axis and excessive cortisol produced by
the adrenal gland. To study the interaction between elevated
stress hormones and the hippocampal function, researchers tested
the cognitive abilities and examined the brain tissue in animal
models of rats with Type 1 diabetes (insulin deficient) and mice
with Type 2 diabetes (insulin resistant).
Researchers found that diabetic animals in both models exhibited
learning and memory deficits when cortisol levels were elevated
due to impaired plasticity and declines in new cell growth. Returning
the levels to normal, however, reversed the negative impact on
the hippocampus and restored learning and memory.
"This advance in our understanding of the physiological
changes caused by excessive production of cortisol may eventually
play a role in preventing and treating cognitive decline in diabetes," said
Mattson, who heads the NIA's Laboratory of Neurosciences.
He and Stranahan explained these findings may also help explain
the connection between stress-related mood disorders and diabetes
found in human population studies.
The NIA leads the federal government effort conducting
and supporting research on the biomedical and social and behavioral
aspects of aging and the problems of older people, including Alzheimer's
disease and age-related cognitive decline. For information on dementia
and aging, please visit the NIA's Alzheimer's Disease Education
and Referral (ADEAR) Center at www.nia.nih.gov/alzheimers
or call 1-800-438-4380. For more general information on research
and aging, go to www.nia.nih.gov.
For information on diabetes, go to the National Institute of Diabetes
and Digestive and Kidney Disease at www.niddk.nih.gov.
The National Institutes of Health (NIH) — The Nation's
Medical Research Agency — includes 27 Institutes and
Centers and is a component of the U.S. Department of Health and
Human Services. It is the primary federal agency for conducting
and supporting basic, clinical and translational medical research,
and it investigates the causes, treatments, and cures for both
common and rare diseases. For more information about NIH and
its programs, visit www.nih.gov.