This story excitedly describes the “remarkable” finding that by deleting an enzyme called BACE1 in a mouse model, researchers were able to stop the amyloid plaques found in the brains of people with Alzheimer’s from developing. The enthusiasm is tempered later in the story, when it is noted that previous advances in treating Alzheimer’s in mice have not translated into success in treating Alzheimer’s in people.
The story tells readers there are BACE1 inhibitors in clinical trials in humans, and quotes the study’s lead researcher as saying these drugs could provide hope for Alzheimer’s patients, “if” they can be used long term and don’t have side effects. But that’s a very big “if.” Missing from the story is this background: a number of BACE1 inhibitors have been studied in human clinical trials and were not found to be effective. In fact, just before this story was published, Merck announced it was halting a BACE1 trial after an interim analysis showed it was unlikely that a positive benefit/risk ratio could be established.
The story also glosses over potential harms.
The public jumps at any hint of a cure for Alzheimer’s, which is the most common cause of dementia. According to this 2017 report from the Alzheimer’s Association, an estimated 5.5 million Americans are living with Alzheimer’s, and 5.3 million of them are age 65 and older. It is the sixth leading cause of death in the U.S. Before people die from the disease, they can live for many years fully dependent on others for their care.
Coverage about Alzheimer’s shouldn’t tease people with unjustified language that pumps up hope for a cure. For more on the importance of context and cautionary language when covering stories like this, read “How to report on preliminary Alzheimer’s research results.”
While this experimental approach is too preliminary to have a price tag, it seems reasonable to expect some mention of cost given that human trials are in progress. That cost is likely to be high given the large sums companies are investing in development. According to one study, Alzheimer’s prevention trials alone “will necessarily involve the enrollment of thousands of subjects, last for years, and incur enormous costs.”
The story says researchers saw “reduced neuron loss and better brain function” in the mice, but there’s no data on the how dramatic these effects were. It leaves a false impression that all subjects experienced significant benefits. In fact behavioral changes were small, with about a 10-percent change in fear conditioning for the only statistically significant result.
The story does not explain that mice without BACE1 have a number of other signs of brain deterioration, show signs of hyperactivity and are prone to long-term depression. The story notes that BACE1 inhibitors are being tested in humans but skips over the fact that at least two clinical trials in humans using BACE1 inhibitors were stopped due to liver toxicity, and that other studies were stopped early due to unspecified, unacceptable side effects.
On the plus side, the story describes how the research was performed and notes that “researchers urge caution with the results as many Alzheimer’s discoveries seem to hold true in mice, then fail in people.” It also quotes a researcher who said that it’s unlikely BACE1 inhibitors would totally halt enzyme production in humans even though the gene that produces the enzyme was deleted in mice.
Those are important points that contradict the overall excitement embedded in the rest of the story, but they don’t arrive until the fifth paragraph.
Near the top of the story we are told: “The deletion of just a single enzyme saw the near total reversal of the deposition of amyloid plaques found in brains of those with Alzheimer’s, improving cognitive functions in the mouse subjects.”
The story did not explain that depleting a marker of Alzheimer’s—the amyloid plaques — is not the same as reversing the disease. The story also leaves out the small size of behavioral benefits observed in the study, which could have been used to explain how a single molecular “fix” may not lead to a benefit. Supporting that concern is Merck’s recent statement that it was halting its BACE 1 trial because of a lack of benefit. That statement wasn’t mentioned in the story.
The story does not do any disease-mongering, but it would have been stronger if it provided data about how many people have Alzheimer’s. It is accompanied by a video that gives some information about Alzheimer’s, such as it’s the most common cause of dementia.
The story has only one source: Riqiang Yan, PhD, who was one of the study’s authors. There are no conflicts identified in the story, and none identified in the study.
The story does not explicitly state there is no cure for Alzheimer’s, and it doesn’t discuss current drug treatments for Alzheimer’s symptoms or other approaches being studied as treatments for Alzheimer’s.
The story explains that the study was done in mice and notes that there are BACE1 inhibitors being tested in humans. It also mentions that researchers “are currently in phase II and, in some cases, phase III clinical trials for the various compounds,” although with no description of what that means in terms of the timeline for drug development.
We would have liked more information on how long it will take for results of these studies to become available, and a caution that an actual treatment is years off at best.
The story makes the approach sound more novel than it really is. What the study showed—for the first time—was that amyloid deposits could be reversed in mice that were bred to slowly stop producing the BACE1 enzyme. Research on BACE1 inhibitors has been going on for years.
The story doesn’t offer much more than what appeared in a news release, although it uses independent quotes obtained from Dr. Yan.
The story echos some of the news release’s hyperbolic language, including the word “hope.” We’re left to wonder the source of the story’s opening word, “remarkable.” The word “remarkably” was used in both the news release and the study to describe certain findings.
Systematic, Criteria-Driven
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