Pravastatin at 10 mg/day does not decrease plasma levels of either amyloid-β (Aβ) 40 or Aβ 42 in humans

被引:34
作者
Ishii, K
Tokuda, T
Matsushima, T
Miya, F
Shoji, S
Ikeda, S
Tamaoka, A
机构
[1] Univ Tsukuba, Inst Clin Med, Dept Neurol, Tsukuba, Ibaraki 3058575, Japan
[2] Shinshu Univ, Sch Med, Dept Internal Med 3, Matsumoto, Nagano 3908621, Japan
[3] Tsukuba Mem Hosp, Tsukuba, Ibaraki 3002622, Japan
关键词
cholesterol; pravastatin; amyloid-beta (A beta) 40; A beta 42; Alzheimer's disease; APOLIPOPROTEIN-E GENOTYPE; ALZHEIMERS-DISEASE; CONTROLLED TRIAL; RISK; PEPTIDE; SIMVASTATIN; INDIVIDUALS; STATINS; ALLELE;
D O I
10.1016/S0304-3940(03)00895-4
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
It has been assumed that statins work as a preventative drug for Alzheimer's disease (AD). Although some epidemiological observations raise doubts to the effectiveness of statins for AD, many in vitro and clinical studies insist on the effectiveness of statins decreasing amyloid-beta (Abeta) levels in medium or blood. To explore the effect of pravastatin on Abeta production, we followed the longitudinal plasma levels of both Abeta 40 and Abeta 42 during the allocation of pravastatin in 46 patients with hyperlipidemia. We found no correlation between plasma cholesterol levels or the decreasing values of total cholesterol and those of Abeta 40 or Abeta 42. Patients having Apolipoprotein E4 (ApoE4) had higher low-density lipoprotein levels and lower AP 40 levels in plasma, suggesting ApoE4 seems to influence plasma AP levels via cholesterol metabolism. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:161 / 164
页数:4
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