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239,242-244 The mechanism by which statins may prevent Alzheimerrsquo;s disease is unclear since little is known about their effects in the brain; however, current hypotheses include the sensitivity of gamma;-secretase to lipid cholesterol content, decreased availability of bioactive isoprenoid precursors of cholesterol (and, consequently, reduced isoprenylation of several intracellular signaling proteins), and altered inflammation or microglial activation in response to statin treatment. 245-247 A novel hypothesis suggests that angiogenesis is involved in the mechanism of Alzheimerrsquo;s disease, and that statins, NSAIDs, histamine H 2 -receptor blockers, and calcium channel blockers may prevent Alzheimerrsquo;s disease through anti-angiogenic mechanisms.

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