Abstract

Abstract

Friday, April 1, 2016

A promising approach


phage  a combining form meaning “a thing that devours,” used in the formation of compound words, especially the names of phagocytes.
—Dictionary.com

Last July, about a month after my diagnosis, I learned about a biotech company called Neurophage, whose ambitious aim was to create an entirely new approach to treating Alzheimer’s. This was around the time I was preparing to launch my blog, and its heading—The Diminishing Window—reflected my sense that it was unlikely a cure would be developed in time to help me or anyone else already diagnosed with the disease. Occasionally I would do a news search for Neurophage, but all that would come up were the same stale articles.
Last week, something fresh did spring up. The website of one of Boston’s public television stations excerpted a section from the book, Brain Storms: The Race to Unlock the Mysteries of Parkinson’s Disease, by John Palfreman, a retired University of Oregon journalism professor who has Parkinson’s himself. (Parkinson’s and Alzheimer’s, as well as a number of other neurodegenerative diseases, share similar features.) Though I was aware that Neurophage was pursuing a novel technique, I didn’t grasp how significant this technique could be until I read Palfreman’s lucid account.
The starting point to understanding this approach is “phages,” shorthand for “bacteriophages”—microbes that live in disparate environments, including human stomachs. Phages were unknown until Beka Solomon, a scientist at Tel Aviv University, discovered them in 2004. She was working on what was called the M13 bacteria, with an eye toward treatments for Alzheimer’s and similar diseases.
According to Palfreman, “She wanted to see if human-made antibodies delivered through the animals’ nasal passages would penetrate the blood-brain barrier and dissolve the amyloid-beta plaques in their brains,” Palfreman wrote, referring to a key feature of Alzheimer’s. “Seeking a way to get more antibodies into the brain, she decided to attach them to M13 phages in the hope that the two acting in concert would better penetrate the blood-brain barrier, dissolve more of the plaques, and improve the symptoms in the mice—as measured by their ability to run mazes and perform similar tasks.”
After repeating the tests many times, the results remained consistent: “The mice showed very nice recovery of their cognitive function,” Solomon told Palfreman. With this as a starting point,
she raised an initial $150,000 from family members and hired the scientist Richard Fischer as her first employee. That was in 2007. In the years that followed, the company raised more than $7 million in venture capital and relocated to Cambridge, Massachusetts, home to a critical mass of biotech researchers. The process of developing a drug is typically lengthy, but by the summer of 2014, with a staff of eighteen, expectations were high. As Palfreman phrased it, the company’s leaders “were hopeful that their new discovery might change medical history.” Solomon commented, “We now potentially have a drug that does everything that the phage could do, which can be delivered systemically and is easy to manufacture.”
The key question, of course, is whether the clinical trials will deliver on their enormous expectations. Much is riding on the outcome.
To read Palfreman’s account in its entirety, do a search for “virus that could cure Alzheimer’s.”

6 comments:

  1. I have read conflicting accounts of whether dissolving amyloid plaques restores brain function or slows down decline. What's your sense of the research?

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    1. Dennis, sorry for my very tardy response to your comment back in early April. I get the sense that there is some genuine optimism about new techniques for dissolving amyloid plaque. And I do find the breadth of approaches encouraging, though I am dubious about any breakthrough drug that could benefit me personally.

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  2. Removing amyloid by any means is highly unlikely to lead to any clinically relevant outcomes. They have all failed and will likely all have the same fate. Why? Wrong target, wrong drug. Acetylated tau is the poisonous protein

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    1. And yet, the studies show removal of this as well. http://www.pbs.org/wgbh/nova/next/body/phage-alzheimers-cure/

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    2. And yet, the studies show removal of this as well. http://www.pbs.org/wgbh/nova/next/body/phage-alzheimers-cure/

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  3. Parkinson's disease is a long-term degenerative disease of the central nervous system that mainly affects the motor system of human body. The symptoms generally come on slowly over time. Affected person should take parkinson's disease treatment

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