Gary Landreth of the Case Western Reserve University School of Medicine and his colleagues may have found a way to reverse Alzheimer’s disease (AD). For now, it’s only been tested in mice but clinical studies in humans will hopefully follow.
AD patients of all species accumulate beta amyloid proteins in their brains. These proteins form plaques that are associated with the cognitive decline seen with this disease. Beta amyloid is naturally cleared from the brain by another protein, apolipoprotein E (apoE). The bad news is that some people, especially those who draw the short genetic straw, don’t make enough apoE to do the job.
Landreth and his team found that a drug called bexarotene dramatically increases the apoE levels. This in turn leads to an almost immediate decrease in the number of beta amyloid plaques in mice. What’s more, mice treated with bexarotene had greatly improved cognitive functions, including memory. For example, AD mice that have been given bexarotene happily went back to constructing nests, whereas untreated mice literally didn’t know what to make of the building materials with which they were provided.
Unfortunately, beta amyloid plaques are only obvious at autopsy. By that time, patients no longer care whether a treatment has potential, and researchers may have had to wait decades to see a result. Mice make much more convenient subjects with their short lifespans and non-litiginous natures. Although bexarotene has a good safety record in humans, we won’t know if it does as well in humans until we try it.