Desmond wondered if their work could be connected to what had happened to him. His firm was an investor in Rapture Therapeutics. Had he discovered something they didn’t want him to know? Could he be part of a clinical trial gone bad?

He continued reading the Rapture website, intrigued by what he learned. The company seemed to be on the cusp of a major breakthrough. Two years ago, Rapture had licensed a therapy that might well hold the key to curing Parkinson’s, Alzheimer’s, Huntington’s, amyloid disorders, and a host of other neurodegenerative diseases.

The key to this potential cure was reportedly discovered by accident. In 2004, an Israeli researcher named Beka Solomon was conducting Alzheimer’s trials when she stumbled onto a new therapy that reduced the brain plaques associated with Alzheimer’s by an astounding eighty percent. That made it far more effective than any treatment on the market.

But Solomon had actually begun her trials with a focus on a completely different therapy. She had genetically engineered mice to develop Alzheimer’s and was treating the mice with a human-derived antibody, which she administered via their nasal passages. The problem was, her therapy didn’t effectively cross the blood-brain barrier and reach the plaques in the parts of the brain affected by Alzheimer’s. In what might go down as one of the greatest twists of scientific luck, Solomon decided to attach her antibody to a virus called M13 to transport it across the blood-brain barrier.

M13 was a special type of virus called a bacteriophage—a virus that infected only bacteria. And M13 infected only one type of bacteria: Escherichia coli, or E. coli. To Solomon’s surprise, the antibody, when attached to M13, showed great success in her trials. But what was truly surprising was that the group of mice treated with the M13 virus alone—without Solomon’s antibody therapy—also showed incredible improvement. It seemed that the positive outcomes from the trials were due entirely to M13, not to Solomon’s actual antibody therapy.

After a year of treatment, the mice that received M13 had, on average, less than a fourth of the plaques of those in the control group. Subsequent experiments showed that M13 could also dissolve other amyloid aggregates—the tau tangles found in Alzheimer’s and the amyloid plaques associated with other diseases, including alpha-synuclein (Parkinson’s), huntingtin (Huntington’s disease), and superoxide dismutase (amyotrophic lateral sclerosis). The M13 phage even worked against the amyloids in prion diseases, a class that included Creutzfeldt-Jakob disease. The discovery was startling and represented a potentially huge breakthrough in the fight against neurodegenerative diseases.

Thus began the long process of trying to figure out how M13 did its miraculous work. After years of research, scientists discovered it was actually a set of proteins—called GP3—on the tip of the M13 virus that was the key to its incredible ability. The GP3 proteins essentially enabled M13 to attach to E. coli and unzip the bacteria, allowing M13 to inject its own DNA inside for replication. And by a stroke of sheer luck, the GP3 proteins also unlocked clumps of misfolded proteins found in Alzheimer’s, Parkinson’s, Huntington’s, and other diseases.