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T he putative potential of statins to retard the onset and progression of Alzheimer disease (AD) remains controversial. Statin therapy may have the potential to increase nonamyloidogenic soluble amyloid precursor protein (sAPP ), thereby reducing -amyloid 42 (A 42) 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. 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 without such mutations but with hyperlipidemia (low-density lipoproteins [LDL] 100 mg/dL) and/or who are heterozygous for apolipoprotein ε4 (APOEε4).

Statins Differentially Affect Amyloid Precursor Protein Metabolism in Presymptomatic PS1 and Non-PS1 Subjects