Barts-MS rose-tinted-odometer ★★★★★
As you know high-dose simvastatin 80-mg per day is being tested in a phase 3 trial in the UK (MS-STAT2). I have referred several patients to participate in this study. Despite this, there has always been a worry about this treatment strategy because statins have been associated with changes in cognition, which is why I have always said that if I needed a statin I would take one that was non-CNS penetrant, for example, pravastatin.
The publication below is reassuring in that it shows that statin therapy in a population of elderly Australians was not associated with any greater decline in memory or cognition over 6 years compared to non-statin users. In fact, statin usage actually attenuated the decline in specific memory test performance in participants with heart disease and the genetic dementia risk factor apolipoprotein Eε4.
You may ask what has this got to do with MS? I think a lot. One of the theories of delayed or late worsening in MS is related to early ageing mechanisms. This is why it will become important in the future to tackle ageing as a potential add-on treatment for MS (please see my previous blog post, ageing, on this topic).
Samaras et al. Effects of Statins on Memory, Cognition, and Brain Volume in the Elderly. Journal of the American College of Cardiology, Volume 74, Issue 21, November 2019 DOI: 10.1016/j.jacc.2019.09.041
Background: There is widespread consumer concern that statin use may be associated with impaired memory and cognitive decline.
Objectives: This study sought to examine the association between statin use and changes in memory and global cognition in the elderly population over 6 years and brain volumes over 2 years. Interactions between statin use and known dementia risk factors were examined.
Methods: Prospective observational study of community-dwelling elderly Australians age 70 to 90 years (the MAS [Sydney Memory and Ageing Study], n = 1,037). Outcome measures were memory and global cognition (by neuropsychological testing every 2 years) and total brain, hippocampal and parahippocampal volumes (by magnetic resonance) in a subgroup (n = 526). Analyses applied linear mixed modeling, including the covariates of age, sex, education, body mass index, heart disease, diabetes, hypertension, stroke, smoking, and apolipoprotein Eε4 carriage. Interactions were sought between statin use and dementia risk factors.
Results: Over 6 years there was no difference in the rate of decline in memory or global cognition between statin users and never users. Statin initiation during the observation period was associated with blunting the rate of memory decline. Exploratory analyses found statin use was associated with attenuated decline in specific memory test performance in participants with heart disease and apolipoprotein Eε4 carriage. There was no difference in brain volume changes between statin users and never users.
Conclusions: In community-dwelling elderly Australians, statin therapy was not associated with any greater decline in memory or cognition over 6 years. These data are reassuring for consumers concerned about statin use and risk of memory decline.