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Douglas A. Hinerfeld, PhD; Majaz Moonis, MD, MRCPI, DM; Joan M. Swearer, PhD; Stephen P. Baker, MScPH; Richard J. Caselli, MD; Ekaterina Rogaeva, PhD; Peter St. George-Hyslop, MD; Daniel A. Pollen, MD

Arch Neurol. 2007;64(11):1672-1673.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

The putative potential of statins to retard the onset and progression of Alzheimer disease (AD) remains controversial.^1-2 Statin therapy may have the potential to increase nonamyloidogenic soluble amyloid precursor protein (sAPP), thereby reducing β-amyloid 42 (Aβ₄₂) and the downstream markers of neurodegeneration phospho-tau (p-tau) and total tau in the cerebrospinal fluid, and thus potentially slow the onset and progression of AD.^3-5 Thus, in a small but unique cohort of cognitively normal subjects with presenilin 1 (PS1) mutations, we have taken the opportunity to conduct an hypothesis-generating pilot study to assess the effects of intensive statin therapy, using both a lipophilic (simvastatin) and a hydrophilic (atorvastatin) statin. We also studied a second group of subjects . . . [Full Text of this Article]

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