Stress Hormone Impacts Memory, Learning in Diabetic Rodents

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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 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 bythe National Institute on Aging (NIA), part of the
National Institutes of Health (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.