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Clinical Trial of Alzheimer's Drug Lecanemab Looks Promising

A new drug appears to slow decline in people with early Alzheimer’s disease.

Key points

  • The amyloid plaques in Alzheimer's disease can be removed from the brain.
  • The clinical decline in Alzheimer's disease can be slowed, but side effects can include brain swelling and brain bleeding.
  • Medications that can slow the decline of Alzheimer's disease are best given as early as possible.

Imagine your doctor tells you that, as part of your annual checkup, you’ll be given a brain scan to see if you are developing the amyloid plaques that cause Alzheimer’s disease. The scan shows you have the plaques. Your doctor tells you not to worry; they’ll simply start you on a drug given twice a month that will remove the amyloid plaques before they damage your brain and prevent you from developing Alzheimer’s disease.

Sound like science fiction? It’s closer than you think.

A new study

A study published in the New England Journal of Medicine and simultaneously presented at the 2022 Clinical Trials on Alzheimer’s Disease conference found that people with early Alzheimer’s disease showed less decline in their cognition and function over 18 months if they were in the group that took the experimental drug lecanemab than if they were in the placebo group. Let’s examine this study to understand what the results mean and how they may impact you or a loved one in the future.

How does the drug work?

Lecanemab is a monoclonal antibody engineered in a laboratory to stick to amyloid protofibrils that clump together with other substances to form plaques in the brains of people with Alzheimer’s. Most researchers believe that the plaques form first and damage brain cells, causing tau tangles to form inside them, killing the cells. Once lecanemab sticks to the plaque, your body’s immune system will come in and remove the plaque, thinking it’s a foreign invader.

Who benefited from the drug?

The 1795 participants in this study had early Alzheimer’s disease, defined as having evidence of amyloid plaques in their brain from either a brain scan or a lumbar puncture, and mild memory problems with either normal daily function (mild cognitive impairment) or difficulty with complicated daily tasks like paying bills and doing shopping (mild dementia). From the race and ethnicity data presented at the conference, the majority of participants in this worldwide study were White (76.9 percent), with most others identifying as either Asian (16.9 percent) or Black (2.6 percent); 12.9 percent identified as Hispanic. The percentages of those identifying as Black and Hispanic were somewhat higher in the US enrolled participants, 4.5 percent and 22.5 percent, respectively.

How well does the drug work?

The group who took the drug lecanemab showed less decline on measures of daily function and cognition compared to the placebo group. The difference in the primary outcome measure was 0.45 on an 18-point scale of clinical status, with scores of 0.5 to 6 indicating early Alzheimer’s disease, the population in the study. A difference of 0.45 may not sound like much, but it was larger than their target of 0.37, which the authors suggest means that this medication produced a clinically meaningful difference in these patients. Another way of looking at it is that that the drug reduced clinical decline by 27 percent. In addition to this primary outcome measure, secondary outcome measures that evaluated activities of daily living and cognition also showed less decline in the lecanemab group, by 37 percent and 26 percent, respectively.

The drug cleared amyloid from the brain to the point that, if the amyloid scan was being done for diagnostic purposes, it would be read as negative (meaning that the person doesn’t have Alzheimer’s disease). Most remarkable from my perspective were the data presented at the conference that lecanemab reduced both total tau (an indicator of the overall damage to the brain) and phosphorylated tau (which forms the tangles in Alzheimer’s disease). These amyloid and tau results suggest that lecanemab can, in a very real sense, reduce the amount of Alzheimer’s pathology that someone has in their brain.

What were the side effects?

44.7 percent of participants in the lecanemab group had an adverse event thought to be related to the study drug, compared to 22 percent of the placebo group. 12.6 percent of the lecanemab group developed brain swelling (called ARIA-E) compared with 1.7 percent of the placebo group. Some 14 percent of the lecanemab group developed a brain bleed compared to 7.7 percent of the placebo group (individuals with Alzheimer’s can develop small, spontaneous bleeds). Headache was also somewhat more common in the lecanemab group (11.1 percent) compared to placebo (8.1 percent). The largest side effect was an infusion-related reaction, present in 26.4 percent of the lecanemab group versus 7.4 percent of the placebo group. Most participants were able to continue the infusions, such that, overall, only 6.9 percent of the lecanemab group discontinued the study drug, compared to 2.9 percent of the placebo group. Deaths were not different between the groups; six people died in the lecanemab group and seven people in the placebo group. Although they occurred after the published study had ended, two patients taking lecanemab and blood thinners died from brain hemorrhages felt due to the study drug.

What happens next?

The drug will next be reviewed by the FDA, possibly as early as January 2023. If approved, it will then be evaluated by the Center for Medicare and Medicaid, to see if Medicare will pay for it and the brain scans needed to confirm that Alzheimer’s disease is present.

What does the future hold?

Based on the results presented in this paper and the conference, I believe that the standard treatment of Alzheimer’s disease will change. If and when this drug becomes available, I will discuss the side effects, possible risks (including brain bleeds), and potential benefits with my patients who have early Alzheimer’s disease. Given the two recent deaths, I will probably advise against using lecanemab in people who are on blood thinners.

What about my science fiction scenario mentioned above? There is a currently enrolling study recruiting individuals who have amyloid plaques in their brains but no symptoms of memory loss, which aims to determine if lecanemab can delay the development of Alzheimer’s disease, or even prevent it entirely. The future is almost here.


van Dyck CH, Swanson CJ, Aisen P, Bateman RJ, Chen C, Gee M, Kanekiyo M, Li D, Reyderman L, Cohen S, Froelich L, Katayama S, Sabbagh M, Vellas B, Watson D, Dhadda S, Irizarry M, Kramer LD, Iwatsubo T. Lecanemab in Early Alzheimer's Disease. N Engl J Med. 2022 Nov 29. doi: 10.1056/NEJMoa2212948. Epub ahead of print. PMID: 36449413.

Shi M, Chu F, Zhu F, Zhu J. Impact of Anti-amyloid-β Monoclonal Antibodies on the Pathology and Clinical Profile of Alzheimer's Disease: A Focus on Aducanumab and Lecanemab. Front Aging Neurosci. 2022 Apr 12;14:870517. doi: 10.3389/fnagi.2022.870517. PMID: 35493943; PMCID: PMC9039457.

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