The accumulation of soluble and insoluble β-amyloid (Aβ) may initiate or accelerate the pathological process of Alzheimer’s disease.
According to a paper published Dec. 29 in The New England Journal of Medicine, researchers have demonstrated through clinical trials that a monoclonal antibody drug, lecanemab, clears amyloid plaques from the brain.
It can slow cognitive decline in patients with early Alzheimer’s disease.
Lecanemab is a humanized IgG1 monoclonal antibody that has a high affinity for soluble protofibrils in Aβ, targeting and removing this material.
Lecanemab was jointly developed by Biogen, a U.S. biotechnology company, and Eisai, a Japanese company.
The primary results of the drug’s Phase 3 clinical trial were published in September, and the newly published paper contains the full trial data.
The trial lasted 18 months and was conducted in 1795 patients aged 50 to 90 years with early stage Alzheimer’s disease (with mild cognitive impairment or mild dementia).
Subjects were randomly assigned in a 1:1 ratio to intravenous lecanemab (10 mg/per kg body weight every 2 weeks) or placebo.
The results showed that lecanemab reduced the overall cognitive decline of patients by 27%.
Side effects of lecanemab also raised concerns, with 26.4% of participants experiencing injection-related side effects and 12.6% experiencing amyloid-related imaging abnormalities (the presence of edema or effusion).
In addition, 13 participants died in the trial (six from the experimental group), although an investigation noted no deaths related to the use of the drug.
Lecanemab is expensive, costing between £10,000 and £30,000 per patient per year.
However, the results of the trial also show that Alzheimer’s disease is either a treatable and preventable disease that could spur the development of other drugs.