A new National Institutes of Health (NIH) study in diabetic rodents has identified a potential mechanism by which stress impairs the cognitive health in people with diabetes.
The study found 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.
Also, when levels of the adrenal glucocorticoid hormone corticosterone (also known as cortisol in humans) get back to normal, the hippocampus recovers its ability to construct new cells and regains the 'plasticity' needed to compensate for injury and disease and adjust to change.
NIA's Mark Mattson, Ph.D., and colleagues in the Institute's Intramural Research Program conducted 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," Nature quoted Richard J. Hodes, M.D., NIA director, as saying.
"Further study will provide a better understanding of the often complex interplay between the nervous system, hormones and cognitive health," he added.
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, controls cortisol production.
Individuals with poorly controlled diabetes often have an overactive HPA axis and excessive cortisol produced by the adrenal gland.
In order to study the interaction between elevated stress hormones and the hippocampal function, the researchers examined the cognitive abilities and studied the brain tissue in animal models of rats with type 1 diabetes and mice with type 2 diabetes.
They found that diabetic animals in both models displayed learning and memory deficits when cortisol levels were elevated due to impaired plasticity and declines in new cell growth.
However, returning the levels to normal reversed the negative impact on the hippocampus by restoring 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.
The researchers said that these findings might also help explain the link between stress-related mood disorders and diabetes found in human population studies.
The study is published in the issue of Nature Neuroscience.