Journal
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
Volume 47, Issue -, Pages 147-155Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pnpbp.2013.03.004
Keywords
Alzheimer's disease; Anesthesia; Kinase; Phosphatase; Tau
Funding
- National Institute of General Medical Sciences [R01GM101698]
- Canadian Institutes for Health Research [MOP-106423, PCN-102993]
- Natural Sciences and Engineering Research Council [354722]
- Canada Foundation for Innovation [23905]
- Fonds de la Recherche en Sante du Quebec [16205, 20048]
- Alzheimer Society of Canada
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Alzheimer's disease (AD) is the most common form of dementia and remains a growing world wide health problem. As life expectancy continues to increase, the number of AD patients presenting for surgery and anesthesia will steadily rise. The etiology of sporadic AD is thought to be multifactorial, with environmental, biological and genetic factors interacting together to influence AD pathogenesis. Recent reports suggest that general anesthetics may be such a factor and may contribute to the development and exacerbation of this neurodegenerative disorder. Intra-neuronal neurofibrillary tangles (NFT), composed of hyperphosphorylated and aggregated tau protein are one of the main neuropathological hallmarks of AD. Tau pathology is important in AD as it correlates very well with cognitive dysfunction. Lately, several studies have begun to elucidate the mechanisms by which anesthetic exposure might affect the phosphorylation, aggregation and function of this microtubule-associated protein. Here, we specifically review the literature detailing the impact of anesthetic administration on aberrant tau hyperphosphorylation as well as the subsequent development of neurofibrillary pathology and degeneration. (C) 2013 Elsevier Inc. All rights reserved.
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