Anesthetics In Alzheimer's

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Inhaled anesthetics commonly used in surgery are more likely to cause the aggregation of Alzheimer's disease-related plaques in the brain than intravenous anesthetics say University of Pittsburgh School of Medicine researchers in a journal article published in Biochemistry. This is the first report using state-of-the-art nuclear magnetic resonance (NMR) spectroscopic technique to explain the detailed molecular mechanism behind the aggregation of amyloid B (AB) peptide due to various anesthetics.
Previous studies by the Pittsburgh researchers found that the inhaled anesthetics halothane and isoflurane and the intravenous anesthetic propofol encouraged the growth and clumping of AB in a test tube experiment.

"Our prior research had shown in molecular models that anesthetics may play a role by causing amyloid peptides to clump together - something that is thought to signal the advancement of Alzheimer's disease. In this study, we set out to see why this was happening and to determine if any one form of anesthesia might be a safer option than another," said Dr. Mandal.

In this study the researchers used NMR spectroscopy to determine how the inhaled anesthetics halothane and isoflurane and the intravenous anesthetics propofol and thiopental interact with AB influencing the aggregation of AB in forms commonly found in the brains of people with Alzheimer's disease. The results were strikingly different between the inhaled and injected anesthetics. The inhaled halothane and isoflurane had the most potent interaction with AB peptides causing the highest levels of AB aggregation. The injected anesthetic propofol only interacted and caused aggregation at high concentrations - interaction was not evident at lower concentrations. The intravenous thiopental did not cause the clustering of AB peptides even at high concentrations. Additionally, the molecular details for the interaction of these anesthetics with AB peptide were revealed.