In spite of the prospects so far, millions of dollars that went into the development of new experimental drugs designed to stop Alzheimer’s in its tracks, and participants’ high hopes, a late-stage medical study on 2016 revealed the scientific hard facts. The experimental drug dubbed solanezumab, researchers said, works no better than a placebo.
In a string of misfortune, drugmaker Merck announced on Tuesday, February 14th, it would stop the development of yet another Alzheimer’s experimental drug called verubecestat, because of its lack of effectiveness.
According to the scientific community, the onset of Alzheimer’s could be traced back to a buildup of a protein called beta-amyloid in the brain, which in turn leads to thinking impairments and memory issues. At the same time, however, there are some that contest the “amyloid hypothesis”.
In spite of the scientists’ efforts, however, no drugs able to at least stall the development of the brain-robbing disease have been successfully developed yet. Another theory suggests attacking the disease by administrating treatments to healthy patients but genetically predisposed to the condition before they exhibit symptoms. Hence, the Banner Alzheimer’s Institute was launched in Phoenix almost a decade ago.
Multiple studies are already testing that hypothesis, including two trials spearheaded by the Phoenix-based institute. The researchers focus on two people who come from two different families who face high genetic risk but no symptoms. One study involves healthy older subjects who face a high genetic risk of developing the condition because of medical family history, while the other one looks at an extended Colombian family predisposed to Alzheimer’s.
Banner Alzheimer’s Institute’s executive director, Dr. Eric Reiman says these trials are not for the faint-hearted as there is no guarantee that the experiments will yield positive results anytime soon. He believes that scientists have a 50-50 percent chance of getting the formula right by 2025.
Talking about the solanezumab disaster, Dr. Reiman says that one potential reason as to why it proved ineffective could have been faulty dosing. Another one of his theories talks about poor timing, saying the drug was administered after the disease already got to inflict a lot of damage to the brain before the treatment could take any effect.
Even though science took a step back, Dr. Reiman believes researchers should continue investigating the effects of anti-amyloid treatments both in Alzheimer’s patients already exhibiting symptoms, as well as in healthy subjects genetically predisposed to the condition.
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