Discovery in Diabetic Rodents May Help in Fight Against Cognitive
Impairment
Increased stress hormone from adrenal gland disrupts healthy
hippocampus
Feb.
18, 2008 - Diabetes, common among senior citizens, is known to impair the cognitive health of people.
But now scientists have identified one potential mechanism underlying
these learning and memory problems. Although the current study used
diabetic rodents, the researchers see a potential for new approaches in
preventing and treating cognitive impairment.
The new
National Institutes of Health (NIH) study 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.
Editor’s Notes
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.
