This past Sunday, the Boston Globe ran a lengthy article devoted to an Eli Lilly drug candidate designed to slow—not cure—Alzheimer’s disease. The article, produced by the news organization STAT, stated that while the drug failed to slow mental and physical deterioration among people with mild-to-moderate Alzheimer’s, the news was not all bad. As the author of the piece, Damian Garde, noted, “a secondary analysis of pooled data in patients with mild forms of the disease” showed a 34 percent reduction in the patients’ cognitive decline.
This finding could be significant. While some people with Alzheimer’s deteriorate rapidly, the much more common scenario is a long, gradual decline—so mild that in the earliest stage of the disease, neither doctors nor patients are likely to be aware that the person has the disease. This is especially true for people with early-onset Alzheimer’s, because they aren’t at an age when the disease is expected to occur, and symptoms are mistaken for other problems, such as attention deficit disorder. In my case, it took about three years from my first symptoms to my diagnosis. Like most people in my situation, I felt that I had been given a death sentence. And I had. But the executioner has turned out to be a lazy fellow, and four-and-one-half years later, my symptoms remain mild.
But there is a possibility that Eli Lilly’s drug candidate, solanezumab, could add many additional years to the arc of Alzheimer’s progression. At the far end of optimism is the notion that Alzheimer’s could become a manageable disease, as AIDS did in the early 1990s, thanks to a complex cocktail of drugs. According to Garde, people treated with solanezumab performed about 35 percent better on cognitive tests than those on a placebo.
In tandem with common-sense measures such as exercising regularly, following a reasonable diet and getting plenty of sleep, solanezumab could extend life expectancy significantly in the face of Alzheimer’s, according to Garde. But as he noted, roughly 99 percent of all Alzheimer’s treatments have failed. A particularly blunt statement came from Mayo Clinic neurologist David Knopman: “I hate having to tell people that we don’t have anything that can truly arrest the disease at this point.” The rather modest aim, according to Garde, is to see if the drug does better than the placebo. The plan is to inject the subjects, all of whom are at a relatively mild stage of Alzheimer’s, once a month with a drug that has the potential to clear away amyloid plaque, a dominant feature of the disease.
As the Alzheimer’s researcher Dr. Howard Fillit commented in Garde’s article, the best-case scenario would be that solanezumab would serve as a foundation for further Alzheimer’s research. That, Fillit said, would likely create the biggest market for any pharmaceutical ever. Under optimal circumstances, the drug could be approved by late next year. That strikes me as a long shot. Still, solanezumab is welcome news.