The current consensus is that Alzheimer’s, a debilitating and progressive condition affecting millions of people and their loved ones, is brought on by an accumulation of amyloid-beta and abnormal tau proteins, which accrete in the brain into neural plaques and neurofibrillary tangles. However, some researchers also believe that cholesterol may be associated with Alzheimer’s, as laboratory animals fed a diet high in cholesterol also had elevated levels of amyloid-beta.

In 2004, at the American Heart Association’s annual Scientific Sessions, research presented by Dr. Larry Sparks provided evidence of this link. Dr. Sparks studied 25 elderly patients with early Alzheimer's symptoms to look for any difference between a placebo group and a group taking Lipitor, one of the commonly used statin drugs that lower cholesterol. 28% of the placebo group managed to stave off any worsening in symptoms after a year, but a significantly higher 53% of those taking Liptor remained stable. In the first three months, scores for memory and cognitive function were close, but as time went on the benefit of Lipitor became more apparent.

This study implied that lowering cholesterol could delay the progression of Alzheimer’s, and in August 2007, a study published by Dr. Gail Li in the journal Neurology provided autopsy evidence to further strengthen these claims. Dr. Li examined the brains of 110 patients and found that while there was no difference in neuronal plaque, patients who had taken statins had far fewer neurofibrillary tangles.

Much about Alzheimer’s remains unclear, including why neural plaques were unaffected by statins in Dr. Li’s study and whether plaques and tangles are even the primary cause of Alzheimer’s. Still, Dr. Li’s autopsies supported previous findings, which were derived from cognitive tests, with physical evidence. If research eventually demonstrates that performance and brain structure are both affected by statins, then a clearer consensus on cholesterol’s link to Alzheimer’s will have been established.