There is currently no cure for Alzheimer’s disease, and while available treatments can temporarily slow the worsening of dementia symptoms and improve quality of life for those suffering from it, they cannot stop the disease from progressing altogether.
But Israeli scientist Beka Solomon may have made a major breakthrough for Alzheimer’s and other brain diseases. The professor, from Tel Aviv University, made an incredible discovery one day when testing a new class of agents against Alzheimer’s disease. The main component is a humble virus scientists refer to as M13, and if successful, it may even mark the beginning of the end of many neurodegenerative diseases.
Of the various forms of viruses, there is one kind that solely infects bacteria. Called bacteriophages, or simply phages, these microbes are more than three billion years old, and reside everywhere on the planet.
M13 is a phage that infects just one type of bacteria, Escherichia coli, or E. coli, found in large quantities within mammalian intestines. The purpose of this phage is to pass on their genes, and in order to do this, they have developed tools to allow them to infiltrate, take over, and kill their bacteria hosts.
It all surfaced in 2004. Solomon was conducting an experiment on a group of mice that had been genetically engineered to develop Alzheimer’s disease plaques in their brains in hopes of seeing whether human-made antibodies delivered through the animals’ nasal passages would penetrate the blood-brain barrier and dissolve the amyloid-beta plaques in their brains. She decided to attach them to M13 phages in an attempt to dissolve more of the plaques and therefore improve the symptoms in the mice.
“The mice showed very nice recovery of their cognitive function,” Solomon explained. In fact, upon examining the brains of the mice, she and her team found that the plaques had been largely dissolved. After running the experiment for a year, Solomon discovered that the phage-treated mice had 80 percent fewer plaques than untreated ones. But how?
While Solomon was unsure, she knew her findings were important, so she decided to patent M13’s therapeutic properties for the University of Tel Aviv. Eventually, in 2007, Solomon’s son, Jonathan Solomon, and fellow Harvard student Hampus Hillerstrom, with $150,000 in seed money contributed by family members, began a new venture, NeuroPhage Pharmaceuticals. Their first order of business was to explore M13’s therapeutic properties.
Researchers at NeuroPhage then discovered something completely unanticipated: the M13 virus was able to dissolve other amyloid aggregates — the tau tangles found in Alzheimer’s and also the amyloid plaques linked to other diseases like alpha-synuclein (Parkinson’s), huntingtin (Huntington’s disease) and superoxide dismutase (amyotrophic lateral sclerosis). The phage proved powerful against the amyloids in prion diseases (a class that includes Creutzfeldt-Jakob disease) as well.
NeuroPhage’s chief scientific officer, Richard Fisher, and his colleagues demonstrated this first by way of test tubes and then in a series of animal experiments. They determined that the M13 virus seemed to possess the properties of a “pan therapy,” which is a universal elixir of the kind the chemist Chris Dobson had once speculated could combat alpha-synuclein for Parkinson’s, as well as amyloids caused by many protein-misfolding diseases at once.
They soon found that M13 phage’s special abilities involved a set of proteins displayed on the tip of the virus, named GP3.
“We tested the different variants for examples of phages with or without tip proteins, and we found that every time we messed around with the tip proteins, it lowered the phage’s ability to attach to amyloids,” explained Rajaraman Krishnan, an Indian postdoctoral student working in an MIT laboratory whom Fisher had recruited to investigate the M13 puzzle.
Fisher found the whole ordeal entirely serendipitous. He said that, by “sheer luck, M13’s keys not only unlock E. coli; they also work on clumps of misfolded proteins.” Fisher explained that the odds of this happening by chance are miniscule. “Viruses have exquisite specificity in their molecular mechanisms, because they’re competing with each other…and you need to have everything right, and the two locks need to work exactly the way they are designed. And this one way of getting into bacteria also works for binding to the amyloid plaques that cause many chronic diseases of our day.”
The team’s next order of business was to see if they could capture the phage’s ability to bust amyloids in a more patient friendly medicine, so they created a new antibody that had the GP3 protein on its surface in order to dissolve amyloid plaques. By 2013, NeuroPhage had tested the new compound, called NPT088, in test tubes and in animals, including nonhuman primates, and found that it performed incredibly well.
So, the big question remains: Will it work in humans?
Although NPT088 is made up of large molecules, it is still fairly poor at penetrating the blood-brain barrier. However, because the medicine persists in the body for several weeks, Fisher believes that, over time, enough can infiltrate the brain to effectively remove plaques.
The hope is to administer the antibody to patients once or twice per month via intravenous infusion for as long as needed.
And if it works, it will undoubtedly change the world. “A single compound that effectively treats Alzheimer’s and Parkinson’s could be a twenty billion-dollar-a-year blockbuster drug,” noted Solomon.
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