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Since CK has\nbeen shown to play a fundamental role in cellular energetics of\nthe brain, any disturbance of this enzyme may exasperate the AD\ndisease process. Mutations in amyloid precursor protein (APP) are\nassociated with early onset AD and result in abnormal processing\nof APP, and accumulation of A<jats:italic>\u03b2<\/jats:italic> peptide, the main\nconstituent of amyloid plaques in AD brain. Recent data on a\ndirect interaction between APP and the precursor of uMtCK support\nan emerging relationship between AD, cellular energy levels and\nmitochondrial function. In addition, recently discovered creatine\n(Cr) deposits in the brain of transgenic AD mice, as well as in\nthe hippocampus from AD patients, indicate a direct link between\nperturbed energy state, Cr metabolism and AD. Here, we review the\nroles of Cr and Cr\u2010related enzymes and consider the potential\nvalue of supplementation with Cr, a potent neuroprotective\nsubstance. As a hypothesis, we consider whether Cr, if given at an\nearly time point of the disease, may prevent or delay the course\nof AD\u2010related neurodegeneration.<\/jats:p>","DOI":"10.1155\/jbb\/2006\/35936","type":"journal-article","created":{"date-parts":[[2006,4,5]],"date-time":"2006-04-05T12:39:24Z","timestamp":1144240764000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":75,"title":["The Creatine Kinase\/Creatine Connection to Alzheimer\u2032s    Disease: CK Inactivation, APP\u2010CK Complexes  and    Focal Creatine Deposits"],"prefix":"10.1155","volume":"2006","author":[{"given":"Tanja 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