Affiliations: [a] Department of General Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China | [b] Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China | [c] Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA | [x] Neurospectroscopy and Neuroimaging Laboratory, National Brain Research Center, Manesar, Gurgaon, India | [y] Department of Neurosciences, Psychiatric and Anesthesiological Sciences, University of Messina, Policlinico G. Martino, Messina, Italy
Correspondence:
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Correspondence to: Cheng-Xin Gong, Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA. Tel.: +1 718 494 5248; Fax: +1 718 494 1080; E-mail: chengxin.gong@csi.cuny.edu.
Abstract: Recent studies have suggested that general anesthesia may initiate or accelerate cognitive impairment and Alzheimer's disease (AD). To understand the possible underlying mechanisms, several studies have been carried out in animal models. In this review, we first briefly discuss the mechanisms leading to neurodegeneration and cognitive impairment in AD, with an emphasis on tau abnormalities in this pathological process. Subsequently, we review the role of anesthesia in inducing tau abnormalities and the possible mechanisms. Recent studies suggest that anesthesia may accelerate the development of AD by promoting abnormal hyperphosphorylation of tau. Further studies are certainly needed to understand the molecular mechanism by which anesthesia may initiate or accelerate cognitive impairment and AD. An understanding of the mechanism will help develop strategies for preventing or eliminating this adverse effect of anesthesia.
Keywords: Alzheimer's disease, anesthesia, phosphorylation, tau
