These authors contributed equally.
Temperature control can abolish anesthesia-induced tau hyperphosphorylation and partly reverse anesthesia-induced cognitive impairment in old mice
Article first published online: 2 SEP 2013
© 2013 The Authors. Psychiatry and Clinical Neurosciences © 2013 Japanese Society of Psychiatry and Neurology
Psychiatry and Clinical Neurosciences
Volume 67, Issue 7, pages 493–500, November 2013
How to Cite
Xiao, H., Run, X., Cao, X., Su, Y., Sun, Z., Tian, C., Sun, S. and Liang, Z. (2013), Temperature control can abolish anesthesia-induced tau hyperphosphorylation and partly reverse anesthesia-induced cognitive impairment in old mice. Psychiatry and Clinical Neurosciences, 67: 493–500. doi: 10.1111/pcn.12091
- Issue published online: 25 OCT 2013
- Article first published online: 2 SEP 2013
- Manuscript Accepted: 12 DEC 2012
- Manuscript Revised: 15 OCT 2012
- Manuscript Received: 10 OCT 2010
- National Natural Science Foundation of China. Grant Number: 30901386
- Wuhan Science and Technology Bureau. Grant Number: 200960323132
- Research Fund for the Doctoral Program of Higher Education of China. Grant Number: 200804871026
- Alzheimer's disease;
- Morris water maze;
- postoperative cognitive decline;
Anesthesia is related to cognitive impairment and the risk for Alzheimer's disease. Hypothermia during anesthesia can lead to abnormal hyperphosphorylation of tau, which has been speculated to be involved in anesthesia-induced cognitive impairment. The aim of this study was to investigate whether maintenance of the tau phosphorylation level by body temperature control during anesthesia could reverse the cognitive dysfunction in C57BL/6 mice.
Eighteen-month-old mice were repeatedly anesthetized during a 2-week period with or without maintenance of body temperature, control mice were treated with normal saline instead of anesthetics. Tau phosphorylation level in mice brain was detected on western blot, and cognitive performance was measured using the Morris water maze (MWM).
After anesthesia-induced hypothermia in old mice, tau was hyperphosphorylated and the cognitive performance, measured on MWM, was impaired. When body temperature was controlled during anesthesia, however, the tau hyperphosphorylation was completely avoided, and there was partial recovery in cognitive impairment measured on the MWM.
Hyperphosphorylation of tau in the brain after anesthesia is an important event, and it might be, although not solely, responsible for postoperative cognitive decline.