Research at Biogen
source: biogen
Alzheimer’s patients who take Leqembi retain the benefits of their treatment even after they stop taking it, latest research Eisai shows.
The Japanese drugmaker and its partner Biogen last week published a further evaluation of clinical trials a monoclonal antibody, also often known as lekanemab. The evaluation showed that Alzheimer’s disease progressed more slowly in patients who took Leqembi, even when they had not used treatment for a mean of two years.
The findings come as drugmakers await a call on full approval of Leqembi. The Food and Drug Administration approved the fast-track treatment in January and is predicted to make a final decision on July 6. The discoveries also come as Eisai and Biogen attempt to get better from the aftermath polarization approval and the disastrous introduction of one other Alzheimer’s therapy, aduhelm, last yr.
About 6.7 million Americans aged 65 and older live with Alzheimer’s disease Alzheimer’s Association. This group is projected to grow to almost 13 million by 2050.
One in three seniors dies of Alzheimer’s or one other form of dementia, which kills more people than breast and prostate cancer combined, the association said. Neurodegenerative disease begins with slight memory loss but ultimately impairs an individual’s ability to think and perform every day activities.
There may be loads of research on Alzheimer’s disease, nevertheless it is amazingly difficult to treat. Many drugs designed to fight the disease have lost in trials. The sheer cost and length of these trials make drug development even harder. And lately, scientists sparked a debate over the true cause of the disease and what medications must be targeted.
In the evaluation, patients with Alzheimer’s disease stopped taking Leqembi after 18 months in the phase 2 clinical trial and later resumed treatment in an extension study. Patients stopped taking Leqembi for a ‘pause period’, which ranged from nine to 59 months before starting it again.
The evaluation compared these patients with a placebo group.
Leqembi reduced amyloid plaque in patients after 12 and 18 months during the clinical trial, in response to the evaluation. Amyloid is a protein that accumulates in the brains of Alzheimer’s patients and disrupts cell function.
The evaluation showed that the reduction in amyloid plaque was accompanied by a “consistent reduction in clinical worsening” in comparison with patients who received a placebo. Which means that Alzheimer’s disease progressed more slowly in patients who received Leqembi compared with patients who took placebo during the clinical trial.
In accordance with the evaluation, the difference in disease progression rates between the Leqembi and placebo groups remained the same during the treatment-free period. In other words, the disease progressed more slowly in the patients who took Leqembi compared with placebo, even when they weren’t taking the medicine.
“The treatment benefits continued,” Dr. David Russell, director of clinical trials at the Institute of Neurodegenerative Diseases, told CNBC.
“The disease has been undone for some time,” he added. “People have one other yr before they progress to a more moderate stage of the disease in comparison with those that haven’t received any treatment.”
Research Institute He’s involved clinical trials of Leqembi and other experimental Alzheimer’s drugs, including donanemab from Eli Lilly and semorinemab from Genentech and AC Immune.
The evaluation showed that patients who took Leqembi also maintained low levels of amyloid plaques during the off period. Protein re-accumulated only barely after patients stopped taking the drug, with a mean increase of about six centiloids. A centiloid is a unit of measure for amyloid in the brain.
That is in keeping with earlier National Institute of Health tests which shows that amyloid is regularly accumulating in the brain.
“It takes many a long time to accumulate enough plaque to begin damaging the brain,” Russell said.
Other Alzheimer’s disease biomarkers proceed to deteriorate
The Alzheimer’s drug Leqembi is seen on this undated news image obtained by Reuters on January 20, 2023.
Hey | via Reuters
But Russell stressed that the lower levels of amyloid plaques seen in people taking Leqembi didn’t mean the disease had stopped progressing. Leqembi and other Alzheimer’s drugs have shown the ability to slow cognitive decline somewhat than stop the disease altogether.
“You do not have to bring the plaque back to the level it was before you began treatment to begin disease progression,” Russell said.
Dr. Lynn Kramer, Eisai’s clinical director of Alzheimer’s disease and brain health, added that “plaque is just part of the whole disease history and process.”
The blood tests in the evaluation showed that other biomarkers of Alzheimer’s disease worsened after stopping treatment, Kramer noted. For instance, one other protein called p-tau181 gathered in the brain, a trend related to cognitive decline.
“These biomarkers are signs of ongoing brain damage and dysfunction,” Kramer said.
“Our data show that discontinuation of therapy after plaque removal will lead to cognitive decline and biomarker disruption in any patient. [monoclonal antibody] unless therapy continues,” he added.
Notably, the evaluation showed that these disease biomarkers improved when patients restarted treatment with Leqembi during the extension study. Amyloid plaques also began to diminish as early as three months after patients resumed taking the drug.
In accordance with the evaluation, this improvement was related to a “greater slowdown” in cognitive decline when treatment was resumed.