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Research at Biogen
Source: Biogene
Alzheimer’s patients who take Leqembi retain treatment benefits even when they stop taking it, new search by Eisai watch.
The Japanese drugmaker and his partner biogenic last week published an additional analysis of the clinical trials of the monoclonal antibody drug, also known as lecanemab. Alzheimer’s disease continued to progress at a slower rate in patients who took Leqembi even when they were off treatment for an average of two years, the analysis found.
The findings come as drugmakers await a decision on whether to fully approve Leqembi. The Food and Drug Administration approved the treatment on an expedited basis in January and is expected to make its final decision on July 6. The findings also come as Eisai and Biogen try to regain their footing after the polarizing endorsement and the disastrous rollout of its other Alzheimer’s treatment, aduhelm, last year.
About 6.7 million Americans ages 65 and older are living with Alzheimer’s disease, according to the Alzheimer’s association. This group is expected to grow to nearly 13 million by 2050.
One in three seniors dies with Alzheimer’s disease or another form of dementia, which kills more people than breast cancer and prostate cancer combined, according to the association. Neurodegenerative disease begins with slight memory loss but eventually impairs a person’s ability to think and carry out daily activities.
There’s a lot of research on Alzheimer’s disease, but it’s notoriously difficult to treat. Several drugs designed to target the disease have failed in the trials. The cost and duration of this research further hampers drug development. And in recent years, scientists have triggered a debate on the real cause of the disease and on the drugs to be targeted.
In the analysis, patients with Alzheimer’s disease stopped taking Leqembi after 18 months in a phase two clinical trial and then resumed treatment in an extension trial. Patients stopped Leqembi for an “off period” ranging from nine to 59 months before restarting the drug.
The analysis compared these patients to a group that received a placebo.
Reduced Leqembi amyloid plaque in patients after 12 and 18 months during the clinical trial, according to the analysis. Amyloid is a protein that accumulates in the brains of patients with Alzheimer’s disease and disrupts cell function.
The analysis indicated that the reduction in amyloid plaque was accompanied by a “consistent reduction in clinical decline” compared to patients who received the placebo. This means that Alzheimer’s disease progressed at a slower rate in the patients who received Leqembi compared to those who took the placebo during the clinical trial.
The difference in disease progression rates between the Leqembi and placebo groups remained the same during the treatment interval period, according to the analysis. In other words, the disease continued to progress more slowly in patients who took Leqembi compared to placebo, even during the period when they were not taking the medicine.
“The benefit that had been derived from the treatment persisted,” Dr. David Russell, director of clinical research at the Institute for Neurodegenerative Diseases, told CNBC.
“The disease receded for a while,” he added. “People have another year before they progress to a milder stage of the disease compared to people who have had no treatment.”
The research institute is involved with clinical trials for Leqembi and other experimental Alzheimer’s drugs, including Eli Lilydonanemab from Genentech and semorinemab from Genentech and AC Immune.
Patients who took Leqembi also maintained low levels of amyloid plaque during the interval period, the analysis noted. The protein reaccumulated only slightly after patients stopped taking the drug, with an average increase of about six centiloids. A centiloid is a unit of measurement for amyloid in the brain.
It is consistent with Before National Institutes of Health research which shows that amyloid accumulates gradually in the brain.
“It takes several decades to build up enough plaque to start damaging the brain,” Russell said.
Other biomarkers of Alzheimer’s disease are getting even worse
Alzheimer’s disease drug Leqembi is seen in this undated image obtained by Reuters on January 20, 2023.
Eisai | via Reuters
But Russell stressed that lower levels of amyloid plaque seen in people taking Leqembi do not mean the disease stops progressing. Leqembi and other Alzheimer’s drugs have been shown to slow cognitive decline, not completely stop the disease.
“You don’t need to get the plaque back to where it was before you took the treatment to start advancing the disease,” Russell said.
Dr. Lynn Kramer, clinical director of Alzheimer’s disease and brain health at Eisai, added that “plaque is just one piece of the whole disease story and process.”
Blood tests in the analysis showed that other Alzheimer’s disease biomarkers worsened when treatment stopped, Kramer noted. For example, another protein called p-tau181 accumulated in the brain, a trend associated with cognitive decline.
“These biomarkers are signs of ongoing brain damage and dysfunction,” Kramer said.
“Our data shows that when you stop treatment after plaque removal, cognitive decline and biomarker disruptions are going to occur with any [monoclonal antibody] unless therapy is continued,” she added.
Notably, the analysis found that these disease biomarkers improved once patients restarted Leqembi during the extension trial. Amyloid plaque also began to shrink after only three months after patients resumed the drug.
These improvements were associated with a “greater slowing” of cognitive decline after restarting treatment, according to the analysis.