A small UCLA study in an animal model of multiple sclerosis showed some improvement in the mice’s walking ability after the researchers gave them a drug that changed gene expression of cells in the brain and spinal cord called astrocytes.
The study is interesting from a basic science perspective and from the perspective of a new idea for a therapy — improving cholesterol synthesis, which cells need to repair their membranes damaged by the disease. But there’s no immediate application for human patients.
The release would have been improved with some discussion of benefits, harms and how this study fits into the bigger picture of MS treatment. On the plus side, the release lists funding sources and gives us some idea of what is novel about the research.
Estimates are that 400,000 people in the United States have a diagnosis of multiple sclerosis. This short release may create false hope by burying the information that a very preliminary pilot study was done on mice. The study points the way to more research, but does not offer anything tangible to any existing patients. The headline promises “repair of damaged nerves” but stops just short of being entirely false by saying there is a “potential pathway” and not a genuine study in human patients with results we can read. The release is a “pathway” to information that doesn’t lead far.
The news release does not discuss potential costs.
The release doesn’t delve into benefits. This sentence came closest to addressing a benefit:
“For multiple sclerosis, specifically, increasing cholesterol synthesis gene expression in astrocytes of the spinal cord can be a pathway to repair nerves that affect walking.”
The research was done in mice, not humans. The astrocytes were from mice. The “gene expression” can be described with quantities, but the release does not give the reader any details. How much did gene expression change? How much improvement did the mice show? Was there a control group of mice?
The release does not explain whether there are any harms from changing the gene expression in the mice, let alone what the potential harms might be in humans.
The release doesn’t inform readers from the outset that this study was in animals and not humans. Ideally, that information would be included in the headline and opening sentence. Further, the release never mentions the limited implications of such research for humans.
There was no disease mongering.
The release lists the funding sources. The authors declared no conflicts of interest in the published study.
The release does not explain the ways that human patients with multiple sclerosis are treated currently, nor does it explain the existing research context clearly. If the small study is showing a new path for research, we need the context that says “up until now, all the research was done in X way.” We aren’t given that here.
This experimental treatment on mice is clearly not available to humans yet.
The release claims that this small animal study points the way to “a more precise, neuroprotective approach than traditional treatments.” It also states that this strategy is “tailored to repair damage for each disability, one at a time, in contrast to a “one size fits all” treatment approach.”
We take this to mean that the “precision” comes from measuring outcomes on specific functions such as walking and eyesight that are affected by the disease, rather than traditional global measures such as number of lesions on an MRI scan or overall functioning.
The headline skirts the edges, by appearing to promise a way to repair nerves in humans when this study is only in mice. But the headline clings to accuracy by using the phrase “potential path.”