Like many neurodegenerative diseases, early diagnosis and treatment of Alzheimer’s disease (AD) can greatly improve quality of life for individuals with the disease. Now, thanks to recent research into a drug called lecanemab-irmb, early Alzheimer’s patients have more promising options than ever before. The drug, known by the brand name Leqembi in the United States, is an antibody that clears the harmful beta-amyloid protofibril. It is designed specifically for the treatment of early AD in hopes of slowing symptom progression. Read on to find out more about the drug’s unique approach to treating AD.
Leqembi Approved for Early Alzheimer’s Patients
Per the Alzheimer’s Association, Leqembi is the “first traditionally approved treatment that addresses the underlying biology of Alzheimer’s and changes the course of the disease in a meaningful way for people in the early stages.” The drug works by lowering protofibril, a particularly harmful type of beta-amyloid. Beta-amyloid is the protein that builds up in the brain of individuals with AD and causes cognitive and functional decline over time.
A press release from the stakeholders behind the latest Leqembi trial, called Clarity AD, explained the mechanism of the global Phase 3 study. The study, which was placebo-controlled, double-blind, parallel-group, and randomized, evaluated 1,795 people with early AD. The trial took place over three years of treatment, evaluating the impact of lecanemab on cognitive decline. The researchers evaluated factors including memory and participants’ abilities to participate in daily activities like chores and hobbies to determine the rate of decline under treatment.
The results were thrilling: After three years of lecanemab treatment, more than half of the patients showed improvement or no decline from baseline. The patients were evaluated using several different Alzheimer’s disease measurement scales.
Clearing Protofibrils in Early Alzheimer’s Patients
Lecanemab is unique in its approach to treating AD. As mentioned above, the drug tackles protofibrils, which are thought to be the most toxic beta-amyloid species that contribute to progressive cognitive decline. Protofibrils can cause neuronal damage in the brain in two ways. First, they increase the formation of harmful beta-amyloid plaques, which accumulate in the brain and contribute to cognitive decline. Protofibrils also spur cognitive decline by directly damaging the communication mechanisms that exist between neurons and other cells. Leqembi is currently the only early AD treatment widely available that supports neuronal function, specifically by clearing protofibrils, which makes it a compelling option for early disease treatment.
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By preventing further neuronal injury from protofibrils, lecanemab may stand to benefit AD patients long after their treatment protocol has ended. Methodical, long-term studies like this one are a powerful reminder that the results of multi-year clinical trials can be well worth the wait.
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