The researchers found that, at baseline, both older and younger rats with lesions showed a similar decline in the release of ACh in the cereberal cortex of the brain.
However, when the rats were presented with a stimulus -- the appearance of darkness and food -- the older rats with lesions reacted very differently when compared with young animals with similar lesions.
The young rats with lesions still showed a significant increase in ACh release of 60 to 120 percent (compared to baseline) when presented with darkness and food. However, the older lesioned rats showed a very weak and insignificant response -- only a 20 to 40 percent increase in ACh release.
The rats with normal brains (no lesions) did not show such a significant difference between young and old rats. The young non-lesioned rats showed an increased ACh release of about 100 to 180 percent when presented with darkness and food, similar to that found in older non-lesioned rats.
Sarter said it was significant that young rats, even when they lost part of their cholinergic sytems due to lesions, were still able to respond robustly to the stimulus of darkness and food. It was only the older rats with lesions who did not respond to the darkness and food stimulus. If something similar happens in humans, it suggests that people with some kinds of pre-existing brain pathologies may not realize it until the aging process starts and it triggers Alzheimer's or other forms of dementia.
"This is something new for us -- to see an interaction between the aging process and a compromised brain," Sarter said. "We believe that people who develop Alzheimer's disease have something wrong with their brain long before the symptoms appear. It is the aging process that then makes the disease appear."
Sarter said it is not yet known exactly what pathologies some people may have in
their brains that lead them to develop Alzheimer's disease as they age. Most
likely,
'"/>
Contact: Martin Sarter
Sarter.2@osu.edu
614-292-1751
Ohio State University
6-Jun-1999