It cannot have escaped our readers' notice that there has been a public increase in the awareness of the impact of dementia on people's lives: politicians have raised concerns about a dementia ‘time bomb’ as a greater number of people live to an older age; and even the 2013 G8 summit declared1 that there was a need for international initiatives to tackle this illness. The inevitable call for more research is underscored by the lack of any new licenced medications for Alzheimer's disease since 2002. There has been much interest in a putative role for statins – which inhibit the HMGCR enzyme, the rate-limiting step in cholesterol production – as retrospective epidemiological data have shown that they can reduce the risk of developing Alzheimer's disease by up to 70%; but, frustratingly, administration of these drugs to those with the illness appears to produce little benefit. Recent data have now shown that the gene encoding this HMGCR enzyme is a potent modifier for the age at onset and rate of conversion from mild cognitive impairment to Alzheimer's disease.2 Indeed, this work would indicate that its G-negative allele is second only to APOE2 as the most common and important protective genetic variant for spontaneous Alzheimer's disease.