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    Studies: The Relationship between Anesthesia and Alzheimer’s

    By Jennifer Huddleston, staff writer     

    A late 2008 study reported that a commonly used anesthetic can produce Alzheimer’s-associated changes in the brains of living animals. Now a new study reports that anesthetics and hypothermia, both of which cause a patient’s body temperature to fall, may cause an increased buildup of “tau”—a protein associated with Alzheimer’s—in brain cells.

    Researchers at Columbia University Medical Center in New York City studied two groups of mice that produce the abnormal tau protein present in Alzheimer’s patients. One group received anesthetics while the other did not and both groups were examined a week later.

    The researchers found that when compared to the non-anesthetized group, the group that had received anesthetics had more clumps of the tau protein. The researchers also noted that mice that displayed advanced signs of Alzheimer’s experienced faster buildup of tau compared to mice in the early stages of the disease.

    “We hope that this research will initiate an interest in taking precautions to limit the impact of anesthesia on this disease,” said Emmanuel Planel, one of the researchers and an assistant professor at Columbia University Medical Center. As noted in the researchers’ findings, general anesthesia has been previously linked to an increased risk of Alzheimer’s disease.

    According to the Alzheimer’s Association, Alzheimer’s is currently the sixth-leading cause of death in the United States and as many as 5 million Americans are currently living with the disease.

    In November 2008, a team of researchers from Massachusetts General Hospital (MGH) in Boston demonstrated for the first time that a common anesthetic—isoflurane—can produce Alzheimer’s-associated changes in the brains of living mice.

    “These are the first in vivo results indicating that isoflurane can set off a time-dependent cascade inducing apoptosis [cell death] and enhanced levels of the Alzheimer’s-associated proteins BACE and A-beta,” said Zhongcong Xie, M.D., Ph.D., the study’s lead and corresponding author.

    Buildup of A-beta plaques in the brain is a key characteristic of Alzheimer’s disease. These plaques are formed when two enzymes—beta-secretase (BACE) and gamma-secretase—clip an amyloid precursor protein (APP) to release the A-beta fragment. In normal brains, APP is processed by another enzyme—alpha-secretase—which produces a non-toxic protein.

    The researchers administered isoflurane to normal mice for two hours at doses similar to what would be given to human patients, then compared the anesthetized mice to a control group two, six, 12 and 24 hours later. Researchers found that the mice given isoflurane had elevated levels of the cell-death protein caspase and increased BACE after six hours. After 12 hours, BACE levels in the treated mice had increased further and caspase activation was still present. Finally, after 24 hours, the anesthetized mice had four-times the levels of BACE as the control mice and their A-beta levels had increased while caspase activation ceased.

    In the same study, a separate group of mice was treated with the drug clioquinol for seven days prior to being given isoflurane. Previous studies have shown that clioquinol hinders the collection of A-beta plaques. Six hours after isoflurane administration, the group that had been treated with clioquinol had lower caspase levels than the group that had received only the anesthetic. This finding supports a 2007 study by the MGH team that found that applying isoflurane to neural cells increased caspase activation and increased levels of BACE and gamma-secretase as part of creating A-beta plaques. Further, these findings provide hope that a drug similar to clioquinol could prevent the harmful effects of isoflurane.

    “This work needs to be confirmed in human studies, but it’s looking like isoflurane may not be the best anesthesia to use for patients who already have higher A-beta levels, such as the elderly and Alzheimer’s patients,” said Xie, an assistant professor of anesthesia at MGH’s Mass General Institute for Neurodegenerative Disease (MGH-MIND), director of the Geriatric Anesthesia Research Unit at the MGH Department of Anesthesia and Critical Care and an assistant professor at Harvard Medical School.

    “Until we can directly asses the impact of isoflurane on biomarkers like A-beta levels in the plasma or cerebrospinal fluid of human patients, we cannot conclusively determine its role in increasing the risk for Alzheimer’s or postoperative dementia,” said Rudolph Tanzi, Ph.D., senior author of the study, the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School and director of the MGH-MIND Genetics and Aging Research Unit.

    The results of the MGH study are published in the December 2008 issue of Annals of Neurology. The findings of the Columbia University Medical Center study are published in the March 2009 issue of The Federation of American Societies for Experimental Biology (FASEB) Journal.

    [1] Mooneyhan, Cody. “Anesthesia or Hypothermia: Warning for Alzheimer’s Patients.” March 11, 2009.
    [2]  Ibid.
    [3]  Ibid.
    [4] McGreevey, Sue. “Common Anesthetic Induces Alzheimer’s-associated Changes in Mouse Brains.” Nov. 12, 2008.
    [5]  Ibid.
    [6]  Ibid.
    [7]  Ibid.
    [8]  Ibid.
    [9]  Ibid.
    [10]  Ibid.

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