In late April, the Tufts University publication TuftsNow showcased the work of the neuroscientist Phil Haydon, an expert on “glial cells,” the most abundant element in the central nervous system. In the past, glial cells were regarded as mere packing material for neuron cells—the cells said to enable cognition.
The TuftsNow article, written by Bruce Morgan, notes that it wasn’t until 2004 that the term “glia” had much relevance for researchers. “Alzheimer’s presents a special case,” Morgan writes, noting that a healthy brain has no trouble regulating the build-up of amyloid plaque. But for those of us who have the disease, the amyloid “overwhelms the brain’s regular maintenance systems with the result that protein fragments accumulate to form hard insoluble plaques.” Over time, cognition declines, with weakening short-term memory typically serving as the canary in the coal mine.
In what Morgan describes as a seminal moment more than two decades ago, Haydon, then doing research at Iowa State University, succeeded in killing off the neurons. “He expected that the glia would fall silent along with the neurons,” Morgan writes. “Instead the glia kept emitting chemical signals…. The glia, Haydon was shocked to discover, were not as passive or inert” as researchers had presumed.
The implications were significant. Over the past decade, Haydon and other researchers have been working on approaches to treat Alzheimer’s and other neurodegenerative diseases. In Haydon’s words, neurons and glia “speak different languages.” In a comparison evoking auto racing, Haydon suggested that the neurons are like the cars in a race, which get all the attention. “But the car needs a pit crew. The pit crew is the glia. They are tuning the brain for peak performance.”
At a conference, Haydon made the point that if he “stimulated the protein in question, it might help clear the excessive level of plaque found among people with Alzheimer’s.” Subsequent testing on mice was encouraging. A particular molecule—identified as GC21109—brought two benefits, according to Morgan. It sped up plaque removal from the brain’s surface and it decreased inflammation.
Phase 1B proof-of-concept trials began in February of last year, involving people with mild or moderate degrees of Alzheimer’s, and the results were promising, Morgan wrote. “According to the usual biomarkers, patients with Alzheimer’s Disease saw rapid reversal of the amyloid cascade” [my italics]. This could lead to a very good thing, but getting through each stage of the regulatory review will take time, and Haydon estimates that the drug won’t be on the market until at least 2022.
This raises a question, maybe a no-brainer question. Should I volunteer for the next round of clinical trials? I seem to meet the criteria. I’m still in the mild stage of Alzheimer’s, and, other than my preexisting disease, I’m in excellent health. And Tufts Medical Center is fairly close to where I live. Most importantly, if the trials are eventually successful, I would have a head start (assuming I have not been taking the placebo). My only reservation is this: Should I qualify for the trial, would I be able to handle the experimental drug’s potential side effects? I certainly hope so.
Mitch, from what you wrote, it sounds as if the researchers would a) evaluate the drug's safety, b) determine a safe dosage range, and c)identify side effects BEFORE the next round of trials. Is that right? Because those three pieces of information would be really valuable to you in deciding whether to volunteer.ReplyDelete
I agree. I've been skittish about volunteering for clinical trials, on account of the unpredictability of the side effects. Since I stopped taking Aricept many months ago, my sleep hygiene has been excellent--eight hours of solid sleep almost every night. Good sleep is fairly high on the list of factors dealing with Alzheimer's.ReplyDelete