London, Feb 18 : A new National Institutes of Health (NIH) tudy in diabetic rodents has identified a potential factor with hich diabetes impairs the cognitive health of people - elevated tress hormones.

The study found that increased levels of a stress hormone roduced by the adrenal gland disrupt the healthy functioning of he hippocampus, the region of the brain responsible for learning nd short-term memory.

Also, when levels of the adrenal glucocorticoid hormone orticosterone (also known as cortisol in humans) get back to ormal, the hippocampus recovers its ability to construct new ells and regains the 'plasticity' needed to compensate for njury and disease and adjust to change.

NIA's Mark Mattson, Ph.D., and colleagues in the Institute's ntramural Research Program conducted the study with Alexis M. tranahan, a graduate student at Princeton University in New ersey.

"This research in animal models is intriguing, suggesting the ossibility of novel approaches in preventing and treating ognitive impairment by maintaining normal levels of lucocorticoid," Nature quoted Richard J. Hodes, M.D., NIA irector, as saying.

"Further study will provide a better understanding of the often omplex interplay between the nervous system, hormones and ognitive healt," he added.

Hypothalamic-pituitary axis (HPA), a hormone-producing system nvolving the hypothalamus and pituitary gland in the brain and he adrenal gland located near the kidney, controls cortisol roduction.

Individuals with poorly controlled diabetes often have an veractive HPA axis and excessive cortisol produced by the drenal gland.

In order to study the interaction between elevated stress ormones and the hippocampal function, the researchers examined he cognitive abilities and studied the brain tissue in animal odels of rats with type 1 diabetes and mice with type 2 iabetes.

They found that diabetic animals in both models displayed earning and memory deficits when cortisol levels were elevated ue to impaired plasticity and declines in new cell growth.

However, returning the levels to normal reversed the negative mpact on the hippocampus by restoring learning and memory.

"This advance in our understanding of the physiological changes aused by excessive production of cortisol may eventually play a ole in preventing and treating cognitive decline in diabetes," aid Mattson, who heads the NIA's Laboratory of Neurosciences.

The researchers said that these findings might also help explain he link between stress-related mood disorders and diabetes found n human population studies.

The study is published in the issue of Nature Neuroscience.

ANI