A breakthrough in the treatment of Alzheimer's: A new drug slows cognitive decline

Are we closer to a cure for the disease?
Ameya Paleja
MRI brain scan
MRI brain scan

haydenbird/iStock 

An antibody therapy that can remove the amyloid toxin in patients with Alzheimer's disease has been shown to slow down the progression of the disease in clinical trials, The Independent reported. This is seen as a major breakthrough in treating the disease after years of scientific research.

Alzheimer's disease is a brain disorder that affects individuals in the latter stages of their life and impacts their memory and thinking ability. In the most severe cases, Alzheimer's patients cannot carry out the simplest tasks. According to estimates from the National Institute of Aging, as many as six million Americans may have dementia caused by Alzheimer's disease.

Scientists do not fully understand the cause of the disease, which makes it difficult to devise a cure. In such a scenario, even a drug that reduces the severity of the disease is hailed as a breakthrough and the results of the recent drug trial demonstrate more than a mere slowdown of disease progression.

What did the trial find?

The trial for the antibody therapy called lecanemab involved nearly 1,800 individuals, aged between 50-90 years, who had been diagnosed with early Alzheimer's disease. The drug was administered to the patients on a fortnightly basis as an intravenous drip for a period of 18 months.

Using a clinical scale, the researchers assessed the severity of dementia by measuring symptoms such as forgetfulness, problem-solving skills, and the ability to live independently. The researchers found that memory decline slowed in patients by 27 percent in those who received the drug. Administering the drug did not halt the disease progression in patients, but it was found to have progressed more slowly in those receiving lecanemab.

During the trial, the researchers also used blood tests and brain scans to measure the levels of amyloid in the patients. In patients that received the antibody drug during the trial, the amyloid levels fell so low that the patients could no longer be clinically diagnosed as affected by Alzheimer's.

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When will the drug be available?

Experts told The Guardian that the drug could provide a real treatment option for the disease and more benefits would become more apparent with time. Other researchers have, however, warned about the risk of adverse events, such as the increased risk of bleeding from using the drug.

During the trial, two participants reportedly died, but the drug manufacturers have claimed that the causes of their deaths were not related to the antibody used. Developed by U.S.-based Biogen and Japanese pharmaceutical company Eisai, the drug will be tested in longer period trials to determine its efficacy and safety, said the research published in the New England Journal of Medicine, released on Tuesday.

The drug maker is also seeking accelerated approval for the treatment with the US FDA as early as march 2023, Interesting Engineering reported in September.

Abstract

BACKGROUND

The accumulation of soluble and insoluble aggregated amyloid-beta (Aβ) may initiate or potentiate pathologic processes in Alzheimer’s disease. Lecanemab, a humanized IgG1 monoclonal antibody that binds with high affinity to Aβ soluble protofibrils, is being tested in persons with early Alzheimer’s disease.

RESULTS

A total of 1795 participants were enrolled, with 898 assigned to receive lecanemab and 897 to receive placebo. The mean CDR-SB score at baseline was approximately 3.2 in both groups. The adjusted least-squares mean change from baseline at 18 months was 1.21 with lecanemab and 1.66 with placebo (difference, −0.45; 95% confidence interval [CI], −0.67 to −0.23; P<0.001). In a substudy involving 698 participants, there were greater reductions in brain amyloid burden with lecanemab than with placebo (difference, −59.1 centiloids; 95% CI, −62.6 to −55.6). Other mean differences between the two groups in the change from baseline favoring lecanemab were as follows: for the ADAS-cog14 score, −1.44 (95% CI, −2.27 to −0.61; P<0.001); for the ADCOMS, −0.050 (95% CI, −0.074 to −0.027; P<0.001); and for the ADCS-MCI-ADL score, 2.0 (95% CI, 1.2 to 2.8; P<0.001). Lecanemab resulted in infusion-related reactions in 26.4% of the participants and amyloid-related imaging abnormalities with edema or effusions in 12.6%.

CONCLUSIONS

Lecanemab reduced markers of amyloid in early Alzheimer’s disease and resulted in moderately less decline on measures of cognition and function than placebo at 18 months but was associated with adverse events. Longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer’s disease.