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Correspondence  |   February 2013
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Author Affiliations & Notes
  • (Accepted for publication October 31, 2012)
    (Accepted for publication October 31, 2012)×
Article Information
Correspondence
Correspondence   |   February 2013
In Reply:
Anesthesiology 02 2013, Vol.118, 466. doi:10.1097/ALN.0b013e31827e3bf1
Anesthesiology 02 2013, Vol.118, 466. doi:10.1097/ALN.0b013e31827e3bf1
Dr. Kopp raises an important point that Dr. Planel and I should have mentioned in our editorial.1  There is no question that mitochondria, reactive oxygen species, and various neurodegeneration pathways, including tauopathy, are linked in some way. And there is also no question that we often treat patients (and animals and cells in our studies) with oxygen as if it is inert. It is most certainly not. However, there is a dearth of literature on the effect of inhaled oxygen on any of the neurodegenerative diseases, so it is not yet clear whether the hypothetical concern raised by Dr. Kopp is real and if so, of what magnitude? Until such data become available, it is important to take Dr. Kopp’s advice and adequately control our studies with respect to oxygen.
Roderic G. Eckenhoff, M.D., Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania. roderic.eckenhoff@uphs.upenn.edu
References
Eckenhoff, RG, Planel, E Postoperative cognitive decline: Where art tau?. Anesthesiology. (2012). 116 751–2 [Article] [PubMed]