This news release from Temple University Health System describes a study in genetically engineered mice showing that an anti-inflammatory asthma drug was able to reverse the impact of particular kinds of brain damage associated with human Alzheimer’s disease and other dementias. The drug, an anti-leukotriene steroid called zileuton, is believed to target the biological pathways involved with damage to “tau” nerve cells in the brain. That damage leads to the fiber-like “tangles” that sabotage the chemical signaling between brain cells needed for learning and memory.
We applaud the release for including the words “in mice” in the headline, something that our reviewers have called the university out for previously. The release would have been strengthened by explicitly addressing the long road still to travel between reversal of tau damage in designer mice and a potential treatment to restore spatial or any other kind of memory in people. A quote noting that the work “could soon be translated” to clinical use was buried at the end of the release, but still left a potentially misleading impression. It also does not mention cost or side effects. The use of use of words like “breakthrough,” and a phrase about “new hope” for patients, detract from the otherwise balanced release.
The U.S. and world public understands the threat of Alzheimer’s disease and other dementias on aging populations. Moreover, to date, these disorders have proven resistant to virtually every medical effort to prevent or treat the devastating loss of cognitive function and overall disability that mark them. Thus, any discovery — no matter how far from actual clinical use — is often the trigger for premature enthusiasm and hype. News release and articles therefore must do their utmost to present findings in cautious context, especially when the research described is in laboratory animals.
At this level of research, speaking to costs would seem to be unnecessary but since the drug used in the study is commercially available, the cost is relevant and should have been mentioned in the release. The drug is expensive — at $500 to $3,000 a month for asthma patients depending on insurance and co-pays — even though it’s impossible to know at this stage what the costs or dosing would be if it is ever proven to be useful in patients with Alzheimer’s disease. Noting the cost could have been done in the context of the costs to care for someone with Alzheimer’s for years or decades.
The release is light on data describing how much better at maze navigation the treated mice were compared to non-treated mice. “… significantly better on the tests…” and “…superior performance do not provide an adequate quantification of the test results. There is also a tacit and unfounded assumption that the reductions in leukotrienes and in tau are sustainable during prolonged treatment.
Harms in a mouse model do not necessarily translate to humans but we do know what the side effects profile looks like. The harms include alteration of liver function, sleep and behavioral disorders — to name a few.
It’s irresponsible to say that this research “could soon be translated to the clinic,” which is simply not true. There’s a tremendous gap between this research and proving clinical effectiveness. As we noted in the summary, the release should have specifically addressed the work still to do in understanding how the reversal of tau damage in designer mice translates to a potential treatment for restoring brain function in people.
No mongering here. But nor does the release provide any context on the prevalence of Alzheimer’s.
Funding sources are named.
The release would have been improved if it had acknowledged the multiple failures over many decades of other once promising drugs for dementia tested in animals. The take-home message should be that these disorders, and brain chemistry in general, are complicated, and although research may bring hope, it has yet to bring effective treatments.
The release makes the statement, albeit at the very end, that the research could “soon translate” into clinical use. That is at best misleading and provides a false hope for patients and their families, given that no timetable or process is given for what would be required to take the step to human use. A plus is that the drug already is approved for use in asthma, but it is likely that even if further animal studies confirm the current work, clinical use is still months or even years away.
The release could have been improved if it noted that the current research is an extension of work done by these researchers. A 2013 publication in PLOS Medicinepreviously demonstrated cognitive improvements in mice treated with zileutin and alterations in levels of tau. The suggestion that this was a breakthrough seems a bit of a stretch given their previous work.
Although parts of the release are cautious in describing what the drug can do, the use of words like “breakthrough” and “especially exciting” appear unwarranted.
This news release from Temple University Health System describes a study in genetically engineered mice showing that an anti-inflammatory asthma drug was able to reverse the impact of particular kinds of brain damage associated with human Alzheimer’s disease and other dementias. The drug, an anti-leukotriene steroid called zileuton, is believed to target the biological pathways involved with damage to “tau” nerve cells in the brain. That damage leads to the fiber-like “tangles” that are suspected of sabotaging the chemical signaling between brain cells needed for learning and memory.
We applaud the release for including the words “in mice” in the headline, something that our reviewers have called the university out for previously. The release would have been strengthened by explicitly addressing the long road still to travel between reversal of tau damage in designer mice and a potential treatment to restore spatial or any other kind of memory in people. A quote noting that the work “could soon be translated” to clinical use was buried at the end of the release, but still left a potentially misleading impression. It also does not mention cost or side effects. The use of use of words like “breakthrough,” and a phrase about “new hope” for patients, detract from the otherwise balanced release.
The U.S. and world public understands the threat of Alzheimer’s disease and other dementias on aging populations. Moreover, to date, these disorders have proven resistant to virtually every medical effort to prevent or treat the devastating loss of cognitive function and overall disability that mark them. Thus, any discovery — no matter how far from actual clinical use — is often the trigger for premature enthusiasm and hype. News releases and articles therefore must do their utmost to present findings in cautious context, especially when the research described is in laboratory animals.
At this level of research, speaking to costs would seem to be unnecessary but since the drug used in the study is commercially available, the cost is relevant and should have been mentioned in the release. The drug is expensive — at $500 to $3,000 a month for asthma patients depending on insurance and co-pays — even though it’s impossible to know at this stage what the costs or dosing would be if it is ever proven to be useful in patients with Alzheimer’s disease. Noting the cost could have been done in the context of the costs to care for someone with Alzheimer’s for years or decades.
The release is light on data describing how much better at maze navigation the treated mice were compared to non-treated mice. “… significantly better on the tests…” and “…superior performance do not provide an adequate quantification of the test results. There is also a tacit and unfounded assumption that the reductions in leukotrienes and in tau are sustainable during prolonged treatment.
Harms in a mouse model do not necessarily translate to humans but we do know what the side effects profile looks like. The harms include alteration of liver function, sleep and behavioral disorders — to name a few.
It’s irresponsible to say that this research “could soon be translated to the clinic,” which is simply not true. There’s a tremendous gap between this research and proving clinical effectiveness. As we noted in the summary, the release should have specifically addressed the work still to do in understanding how the reversal of tau damage in designer mice translates to a potential treatment for restoring brain function in people.
No mongering here. But nor does the release provide any context on the prevalence of Alzheimer’s.
Funding sources are named.
The release would have been improved if it had acknowledged the multiple failures over many decades of other once promising drugs for dementia tested in animals. The take-home message should be that these disorders, and brain chemistry in general, are complicated, and although research may bring hope, it has yet to bring effective treatments.
The release makes the statement, albeit at the very end, that the research could “soon translate” into clinical use. That is at best misleading and provides a false hope for patients and their families, given that no timetable or process is given for what would be required to take the step to human use. A plus is that the drug already is approved for use in asthma, but it is likely that even if further animal studies confirm the current work, clinical use is still months or even years away.
The release could have been improved if it noted that the current research is an extension of work done by these researchers. A 2013 publication in PLOS Medicine previously demonstrated cognitive improvements in mice treated with zileutin and alterations in levels of tau. The suggestion that this was a breakthrough seems a bit of a stretch given their previous work.
Although parts of the release are cautious in describing what the drug can do, the use of words like “breakthrough” and “especially exciting” appear unwarranted.
Systematic, Criteria-Driven
Don’t believe everything you hear, kids.
“What in the world justifies rushing a 348-word story to publication on a Sunday without doing extra research and reporting? Just because a scientist said it? COVID-19 journalism that devolves to that level of dreck is dangerous.”
🔥👇 https://twitter.com/garyschwitzer/status/1268175065478320131
.@Reuters: why rush to publish a 348-word story claiming #COVID19 is losing potency without doing extra research and reporting? Just because a scientist said it? #COVID19 journalism that devolves to that level of dreck is dangerous. https://www.healthnewsreview.org/2020/06/reuters-report-is-another-classic-case-study-in-how-not-to-cover-covid-19-news/
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