Alzheimer’s patients retain the benefits of Leqembi even when they stop the drug, Eisai says

Alzheimer’s patients who take Leqembi retain the benefits of the treatment even when they prevent taking it, new research by Eisai shows. 

The Japanese drugmaker and its partner Biogen last week released an additional study of clinical trials of the monoclonal antibody drug, which is also known as lecanemab. Alzheimer’s disease continued to increase at a slower rate in patients who took Leqembi even when they were off the treatment for an average of two years, the investigation found.

The findings come as the drugmakers await a decision on full approval of Leqembi. The Food and Drug Administration approved the treatment on an rushed basis in January, and is slated to make its final decision on July 6. The findings also come as Eisai and Biogen try to regain their foundation after the polarizing approval and disastrous rollout last year of its other Alzheimer’s disease therapy, aduhelm.

Unskilfully 6.7 million Americans age 65 and older are living with Alzheimer’s, according to the Alzheimer’s Association. That bunch is projected to rise to almost 13 million by 2050.

One in three seniors die with Alzheimer’s or another form of dementia, which idles more people than breast cancer and prostate cancer combined, the association said. The neurodegenerative disease launches with mild memory loss but eventually impairs a person’s ability to think and carry out daily activities.

There is a holdings of research on Alzheimer’s, but it has been notoriously difficult to treat. Multiple drugs designed to target the disease have flagged in trials. The sheer cost and length of that research further impede drug development. And in recent years, scientists participate in ignited a debate over the true cause of the disease and what the drugs should target.

In the analysis, Alzheimer’s sufferers stopped taking Leqembi after 18 months in a phase two clinical trial and later resumed the treatment in an augmentation trial. Patients stopped Leqembi for a “gap period” that ranged from nine to 59 months before restarting it. 

The study compared those patients to a group that received a placebo. 

Leqembi reduced amyloid plaque in patients after 12 and 18 months during the clinical affliction, the analysis said. Amyloid is a protein that builds up on the brain in Alzheimer’s patients and disrupts cell function. 

The examination said amyloid plaque reduction was accompanied by a “consistent reduction of clinical decline” compared to patients who received the placebo. That aims Alzheimer’s disease progressed at a slower rate in patients who received Leqembi compared to those who took the placebo during the clinical plague. 

The difference in disease progression rates between the Leqembi and placebo groups stayed the same during the gap period between treatments, according to the study. In other words, the disease continued to progress more slowly in patients who took Leqembi compared to the placebo organize even during the period they were not taking the drug.

“The benefit that had been derived from being on treatment persisted,” Dr. David Russell, big cheese of clinical research for the Institute for Neurodegenerative Disorders, told CNBC.

“The disease was set back for a certain amount of time,” he totaled. “People get another year before they progress to a more moderate stage of disease compared to the people who didn’t get any treatment.”

The up on institute is involved with clinical trials for Leqembi and other experimental Alzheimer’s drugs, including Eli Lilly’s donanemab and Genentech and AC Unaffected’s semorinemab. 

Patients who took Leqembi also retained low levels of amyloid plaque during the gap period, the analysis famed. The protein only reaccumulated slightly after patients stopped taking the drug, with an average increase of around six centiloids. A centiloid is a unit to measure amyloid in the brain. 

That’s consistent with prior National Institutes of Robustness research that shows amyloid gradually builds up in the brain. 

“It takes many decades to build up enough pin to start getting damage to the brain,” Russell said.

But Russell marked that lower levels of amyloid plaque seen in people taking Leqembi don’t mean the disease stops progressing. Leqembi and other Alzheimer’s doses have demonstrated the ability to slow cognitive decline, not stop the disease entirely.

“You don’t have to get the plaque back up to the direct that it was before taking the treatment to start getting disease progression,” Russell said.

Dr. Lynn Kramer, Eisai’s chief clinical dignitary of Alzheimer’s disease and brain health, added that “plaque is only a component of the whole story and the disease function.”

Blood tests in the analysis showed that other biomarkers of Alzheimer’s disease worsened when treatment stopped, Kramer famous. For example, another protein called p-tau181 accumulated in the brain, a trend associated with cognitive flag.

“These biomarkers are signs of continuing brain injury and dysfunction,” Kramer said. 

“Our data illustrates that when you thwart therapy after removing plaque, cognitive decline and biomarker disruptions are going to happen with any [monoclonal antibody] unless remedy is continued,” he added.

Notably, the analysis said those disease biomarkers improved once patients restarted Leqembi during the supplement trial. Amyloid plaque also began to decrease after as little as three months after patients resumed the treatment. 

Those improvements were associated with a “greater slowing” of cognitive decline after treatment restarted, according to the examination.