Mice don't naturally get Alzheimer's, so the animals in this study were genetically engineered to express the human protein responsible, called amyloid beta. "These mice develop a syndrome with many features of the human disease," explains Eckenhoff. Post-doctoral fellow and first author Shannon Bianchi, MD, exposed "middle-aged" Alzheimer mice to anesthetics at low to moderate concentrations for two hours a day over a total of five days, not unusual for a clinical scenario. The cognitive abilities of the mice were then analyzed using standard behavioral tests, and their brains were examined for plaque and cell death.
"Compared to controls, the anesthesia did not appear to worsen cognitive ability, which was already considerably compromised at this age, but it did accelerate amyloid beta aggregation and plaque appearance," said corresponding author Maryellen Eckenhoff, PhD. "We need to test whether anesthetic at earlier, presymptomatic stages, might accelerate both cognitive loss and plaque." This is the main cause of concern because a large fraction of clinical patients receiving inhaled anesthetics during surgery are older, but presymptomatic individuals.
Are there anesthetics that do not accelerate plaque? "We think so, but far more research is necessary to show this with any confidence. We have to take this one step at a time a problem has still not been demonstrated in humans". It is important to remember that this effect is likely to be subtle, especially with brief surgical procedures, so the risk of not having needed surgery may exceed any potential risk from this still unproven effect. But this latest study adds a little urgency to the effort to find out. "If inhaled anesthetics are contributing to the rise and early onset of this devastating disease then we need to know, and soon," concludes Eckenhoff.
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Contact: Rick Cushman
rick.cushman@uphs.upenn.edu
215-349-5659
University of Pennsylvania School of Medicine
9-Mar-2007