The gene that is responsible for increasing the likelihood of early-onset Alzheimers disease (called APOE-e4) is an apolipoprotein. This means that it contains a lipid-protein combination. And its been argued that the bad low-density lipoprotein (LDL) is involved in the early stages of Alzheimer's disease. Accordingly, scientists from the Boston Collaborative Drug Surveillance Program carried out an analysis to see if there were possible effects of drugs that interfere with blood lipid levels on the risk of developing Alzheimers disease or other forms of dementia.

They used a database of medical information from over 3 million people enrolled by family physicians in the UK. Three groups of subjects were selected from this database.

Group I were all those aged 50 to 89 who had been prescribed a lipid-lowering medication at any time; they were divided into those taking a 'statin'-type drug, and those taking another form of lipid-lowering drug. (The statin drugs are chemically similar, and work directly in the liver to block a substance needed to manufacture cholesterol. They also help the body remove cholesterol from arterial deposits, slowly unplugging blood vessels.)

Group II consisted of patients diagnosed as having increased blood lipid levels but who were not given any medication for it. Group III was a random sample of 25,000 people who were not included in Groups I or II. All the selected people were followed closely for six years, from 1992 to 1998.

All those who developed dementia of any kind were identified, and, for each, up to 4 of the remaining subjects were chosen to match the individual according to age, sex, the date of dementia diagnosis, the physicians practice, and so on. This allowed a fair comparison between those with dementia and those without.

There were almost 25,000 individuals in Group I, over 11,000 in Group II, and, by design, 25,000 in Group III. A total of 284 people had dementia diagnosed for the first time during the six-year period, and theses were matched with 1,080 control subjects. After adjusting for age, sex, date of diagnosis, smoking, body mass index (BMI), previous heart diseases and diabetes, the likelihood of developing dementia was calculated for Groups I and II, compared with Group III people.

The likelihood of developing dementia in people taking statin drugs was only 30% of that in those not taking them; this finding was highly significant. On the other hand, there was no statistical difference for people taking other types of lipid-lowering drugs. Furthermore, the condition of having raised blood lipids did not alter the chance of developing dementia.

These results show that statin drugs appeared to have a protective effect in reducing the likelihood of dementia. It is not clear whether there was a difference in their effectiveness in preventing Alzheimer disease as opposed to vascular dementia, but the majority of the cases were Alzheimers. There was no indication that any of the 5 statin drugs prescribed was more (or less) effective than the others.

This type of analysis, which is called a retrospective observational epidemiological study, does not provide proof that statins are an effective preventative. However, many such studies have been done for other relationships where results have led to the institution of more rigorous, prospective studies. The results of this analysis are sufficiently compelling to justify a large prospective study. In the meantime, all one can say is that the use of statin drugs to treat high lipid levels may have an additional benefit beyond just lowering your cholesterol. Statins are a remarkable class of drugs, and they will most likely provide the basis for the discovery and development of other, more specific types of medication for a variety of diseases.