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AD is an age\u2010associated neurodegenerative disorder characterized pathologically by elevated oxidative stress and subsequent damage to proteins, lipids, and nucleic acids, appearance of neurofibrillary tangles and senile plaques, and loss of synapse and neuronal cells. It is unclear if development of a hypometabolic environment is a consequence of or contributes to AD pathology, as there is not only a significant decline in brain glucose levels in AD, but also there is an increase in proteomics identified oxidatively modified glycolytic enzymes that are rendered inactive, including enolase. Previously, our laboratory identified \u03b1\u2010enolase as one the most frequently up\u2010regulated and oxidatively modified proteins in amnestic mild cognitive impairment (MCI), early\u2010onset AD, and AD. However, the glycolytic conversion of 2\u2010phosphoglycerate to phosphoenolpyruvate catalyzed by enolase does not directly produce ATP or NADH; therefore it is surprising that, among all glycolytic enzymes, \u03b1\u2010enolase was one of only two glycolytic enzymes consistently up\u2010regulated from MCI to AD. These findings suggest enolase is involved with more than glucose metabolism in AD brain, but may possess other functions, normally necessary to preserve brain function. This review examines potential altered function(s) of brain enolase in MCI, early\u2010onset AD, and AD, alterations that may contribute to the biochemical, pathological, clinical characteristics, and progression of this dementing disorder.<\/jats:p>","DOI":"10.1111\/j.1471-4159.2009.06397.x","type":"journal-article","created":{"date-parts":[[2009,9,23]],"date-time":"2009-09-23T09:03:53Z","timestamp":1253696633000},"page":"915-933","source":"Crossref","is-referenced-by-count":158,"title":["Multifunctional roles of enolase in Alzheimer\u2019s disease brain: beyond altered glucose metabolism"],"prefix":"10.1111","volume":"111","author":[{"given":"D. Allan","family":"Butterfield","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miranda L. 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