Alzheimer’s Drug Breakthrough? Maybe — But There Are Some Issues

Alzheimers

Lecanemab may not do enough, and its rollout could be long and challenging. Photo: OsakaWayne Studios/Getty Images

Longevity may be the most important trend we’ve ever experienced. It’s driven by — and in turn, it affects — everything from health to housing, money to technology, lifestyle to social policy. There’s so much to be aware of — and it’s just getting started! Now you can keep up with all the latest developments in this weekly column.

 

An experimental drug  has been found that can apparently slow the rate of decline in Alzheimer’s patients.

As reported here, lecanemab is an antibody targeting the amyloid protein clumps associated with Alzheimer’s. In a global trial involving 1,800 people with early stage Alzheimer’s disease, the patients receiving the drug showed a 27 per cent slower disease progression than those who received a placebo.

In the study, the progression of the disease was tracked “using the clinical dementia rating scale, which scores the patients on cognition and ability to live independently. The participants’ brains were also scanned for the two proteins commonly associated with Alzheimer’s disease: amyloid and tau.”

In both groups, lecanemab and placebo, Alzheimer’s scores worsened during the course of the study, but the rate of decline was slower for those who received lecanemab.

The article notes:

“For the first time, we have a potential treatment that has a demonstrated effect on both the symptoms and underlying pathology of Alzheimer’s disease. These results are a breakthrough in the search for a treatment for this devastating disease and give a strong indication that the course of the disease can be altered.”

However, there are some important “buts”:

  • The rate of slowdown, while statistically significant enough to not be due chance, was still small — only a 0.45 reduction on an 18-point scale
  • There were side-effects. About one in four people in the lecanemab group experienced brain swelling or a bleed on the brain. Two patients died, possibly due to the interaction of the lecanemab with other drugs they were already taking, such as blood-thinner medication. Given that if lecanemab works, the patient may be on it for the rest of their life, these other potential interactions would need to be studied further and better understood
  • There are underlying issues with how Alzheimer’s is diagnosed in the first place that could affect the rollout of such a drug. Eligibility for the trial depended on detection of a sufficient level of amyloid in the brain or spinal fluid, which in turn requires a PET brain scan or lumbar puncture — not easy to implement on a wide scale. The article quotes Dr. Susan Kohlhaas, Director of Research at Alzheimer’s Research U.K.: “We estimate that unless there are drastic changes in how people access specialist diagnostic tests for Alzheimer’s disease, only two per cent of the people eligible for drugs like lecanemab will be able to access them”

In many ways, this story exemplifies some of the challenges in reporting so-called breakthroughs — particularly challenges for laymen like me. The news is often a combination of exciting new potential plus not-so-fast reality. Overall, my mood is resolutely optimistic, because the sheer quantity of new discoveries (even if many are embryonic and require much more work, or don’t pan out at all) increases the odds of exciting new solutions.

The manufacturer has applied to the U.S. Food and Drug Administration for accelerated approval of lecanemab, with a decision expected next month. I’ll keep an eye on the progress.

David Cravit is a Vice-President at ZoomerMedia, and Chief Membership Officer of CARP. He is also the author of two books on the “reinvention” of aging. You can check out some of his other writing here.