TY  - JOUR
T1  - STatins differentially affect amyloid precursor protein metabolism in presymptomatic ps1 and non-ps1 subjects
AU  - Hinerfeld DA, Moonis M, Swearer JM, et al
Y1  - 2007/11/01
N1  - 10.1001/archneur.64.11.1672
JO  - Archives of Neurology
SP  - 1672
EP  - 1673
VL  - 64
IS  - 11
N2  - 
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 α (sAPPα), 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 without such mutations but with hyperlipidemia (low-density lipoproteins [LDL]>100 mg/dL) and/or who are heterozygous for apolipoprotein ε4 (APOEε4).

SN  - 0003-9942
M3  - doi: 10.1001/archneur.64.11.1672
UR  - http://dx.doi.org/10.1001/archneur.64.11.1672
ER  -