Statins and cognitive function
- Sun Health Research Institute, Sun City, AZ, USA
- Dr Larry Sparks, Sun Health Research Institute, 10515 W. Santa Fe Drive, Sun City, AZ 85351, USA; larry.sparks{at}bannerhealth.com
- Received 24 September 2008
- Revised 24 September 2008
- Accepted 25 September 2008
Breteler and colleagues1 have provided us with data indicating a reduction in the risk of incident Alzheimer’s disease (AD) with elective statin use in the largest cohort investigation to date (see page 13). The main preplanned secondary analyses were designed to answer whether an individual’s Apolipoprotein E (ApoE) genotype influenced the benefit of statin treatment and determined if there was a difference in risk reduction based on the blood–brain barrier (BBB) permeability of the statin prescribed. They are the first to report that statin treatment reduced the risk of incident AD regardless of ApoE genotype. They also indicate that there was no significant difference in the reduced risk produced by simvastatin (39%) and pravastatin (62%), although the effect was more prominent with pravastatin, a more BBB-impermeable agent. The two most recent published cohort studies considered atorvastatin as less lipophylic than the current study—but also reported that BBB permeability did not influence the beneficial effect of statin therapy on risk of incident dementia.2 3
It is of note that the last three large cohort studies of over 10 000 total subjects (1674 subjects,2 2068 subjects,3 and current largest study, 6992 subjects)1 found the same effect of reduced risk of incident AD with elective statin use while employing the more rigorous hazard ratios (HR) assessment. In contrast, the next most recent cohort study of 929 subjects4 reported no significant reduction in the HR of incident AD, which was not influenced by ApoE genotype but did identify a reduction in the incidence of senile plaques in statin users.
The current report is the culmination of over a …
