The long goodbye of Alzheimer's disease may become increasingly common as our population ages in coming years, but scientists in Seattle provide reassuring evidence that at least some of the disease's gradual mental decline can be held off with, of all things, cholesterol-lowering drugs.
In a study of 110 elderly volunteers, aged 65 to 79, who donated their brains for research and whose cognitive functions were monitored over several years prior to their death, scientists led by Dr. Eric Larson of the Group Health Center for Health Studies found that those who had taken statin drugs to lower their cholesterol had fewer nerve-damaging plaques and tangles protein deposits that form in and around neurons in their brains than those not taking the medications. Buildup of these protein plaques and tangles are the hallmark of Alzheimer's disease; they inexorably disrupt the critical connections between neurons that govern thought processes and sabotage everything from the storage and retrieval of memories to learning and language skills.
The new findings are the latest and most definitive results linking the popular statin drugs to Alzheimer's. Earlier studies had produced conflicting results: some found that statins reduced the risk of the brain disorder, while others found no effect. Larson's study is the first to directly compare the brains, on autopsy, of statin users and non-users (Alzheimer's can be conclusively diagnosed only after death, when pathologists confirm the presence of the plaques and tangles in the brain). "This data does give us some additional hope that statins may turn out to have a useful relationship in slowing Alzheimer's disease," says William Thies, vice president of medical and scientific relations of the Alzheimer's Association.
How do cholesterol-lowering drugs work on the brain? As experts learn more about Alzheimer's, they believe that it's less a disease of the brain than of the vasculature, or blood vessel system. It turns out that many of the risk factors for Alzheimer's are the same ones for heart disease, and that the build up of protein in the brain is not unlike the gradual accumulation of plaque in the heart vessels. "We are learning that Alzheimer's disease isn't just plaques and tangles appearing through a series of biochemical processes, but that vascular stress may play a role in their development," says Larson. "Anything we can do to lower the vascular risk profile could lower the risk of Alzheimer's." Statins, then, could be inhibiting the development of Alzheimer's by keeping the brain's neural highways free of potentially bottlenecking protein plaques. In addition, says Larson, statins may be working on a more molecular level, by actually blocking the formation of the sticky, fibrous tangles that can jam nerve connections.
To learn more about exactly how statins could be thwarting the Alzheimer's disease process, Larson acknowledges that the first step involves having another, independent group replicate his team's findings. In the meantime, he plans to continue his study by adding more volunteers. Within the next year, Thies expects two more trials to produce results and hopefully solidify the effect statins have on the brain.