New Alzheimers Drug Slows Mental Decline by 27 in Clinical

New Alzheimer’s Drug Slows Mental Decline by 27% in Clinical Trial – Freethink

Japanese pharmaceutical company Eisai and its partner, Cambridge-based Biogen, have announced their drug slowed cognitive decline in Alzheimer’s in a global study.

The drug, an antibody called lecanemab, slowed the rate of cognitive decline by 27% in volunteers compared to those given a placebo in the large late-stage study.

The companies plan to present full study results on November 29 at the Clinical Trials on Alzheimer’s Congress (CTAD), pending publication in a peer-reviewed journal; For now, the release of top-line data is basically all we know.

Eisai and Biogen have announced that their Alzheimer’s drug reduces cognitive decline by 27% in a clinical trial.

A Scientific Cemetery: Any sign of advances in the treatment of Alzheimer’s puts scientists, doctors, patients and advocates on high alert. Previous drugs have either not worked, or have provided murky results at best — as was the case with Biogen’s earlier, controversial Alzheimer’s drug aducanumab.

The field is a therapy cemetery.

Despite the setbacks, researchers have worked doggedly on treatments for decades, and the need is great — and will only increase as the population ages. The Alzheimer’s Association estimates that the number of Americans who will have the disease will be 6.5 million in 2022; By 2050, they predict that the number of people over 65 with Alzheimer’s will almost double to 12.7 million.

The results of the lecanemab study “represent an important milestone for Eisai in fulfilling our mission to meet the expectations of the Alzheimer’s community,” said Haruo Naito, CEO of Eisai.

“Alzheimer’s disease not only poses a major challenge for patients and their families, but also negatively impacts society, including reduced productivity, rising welfare costs and disease-related anxiety. We believe alleviating these burdens will have a positive impact on society as a whole.”

The drug is an antibody designed to attach to a protein in the brain that’s been linked to Alzheimer’s disease.

The drug: The drug is an antibody developed by Eisai and Swedish biotech BioArctic.

While we usually think of antibodies for bacteria or viruses, these Y-shaped proteins can be tuned to stick to numerous targets. In this case, lecanemab is designed to attach to a protein in the brain that has been linked to Alzheimer’s disease.

A clinical hallmark of Alzheimer’s is the build-up of two proteins in the brain called plaques and tangles. A protein called amyloid-beta (Aβ) forms plaques, while another protein called tau creates the tangles. Amyloid has long been the frontrunner in the search for a cause of Alzheimer’s, with the amyloid hypothesis receiving the lion’s share of scientific attention and capital.

The new antibody binds to and clears the amyloid-beta (Aβ) aggregates in the brain, which many researchers believe cause neurodegeneration. The idea is that the antibody may help slow or delay mental decline. Unlike the previously approved Aduhelm, Lecanemad targets the proteins before they clump together, Portal reported.

The study: The study, called Clarity AD, was a phase 3, placebo-controlled, double-blind, randomized trial designed to test whether the drug works.

The 1,795 patients had early Alzheimer’s disease and were randomly divided into placebo and antibody groups, with neither the patients nor the researchers knowing who got what. The treatment group received lecanemab 10 mg intravenously every two weeks.

According to the companies, the group included patients with a variety of comorbidities, including diabetes, heart disease and obesity, as well as diverse ethnic and racial groups.

According to the companies, the group included patients with a variety of comorbidities, including diabetes, heart disease and obesity, as well as diverse ethnic and racial groups.

“Because of the inclusive eligibility criteria and successful recruitment of diverse ethnic and racial populations in the United States, Clarity AD’s population is generally comparable to the country’s Medicare population,” the companies stated.

To assess the progression of neurodegeneration, researchers used the Clinical Dementia Rating-Sum of Boxes (CDR-SB) model.

The results: Eisai and Biogen came to their conclusion – that the antibody slowed the decline compared to the placebo – using the results of the CDR-SB.

As STAT explained, lecanemab patients had a 0.45-point difference over placebo on the 18-point CDR-SB scale at month 18 — a 27 percent reduction in the rate of cognitive decline.

According to the companies, statistically significant differences (ie “distinguishable from random noise”, not necessarily clinically meaningful) were already observed between the groups after 6 months of treatment.

No patient saw their cognition scores improve; The drug is not intended to make people better, but to slow their deterioration.

Regarding the drug’s safety, 12.5% ​​of treatment patients had signs of swelling in the brain – a common side effect of these types of therapies, FierceBiotech found – but only 2.8% showed symptoms.

The Alzheimer’s Association estimates that by 2050, 12.7 million Americans over the age of 65 will have the disease.

The results are “the first definitively positive large clinical trial showing that you can actually slow Alzheimer’s disease at this very early symptomatic stage,” Ivan Cheung, Eisai’s chairman and chief executive officer, said in a reporter’s briefing, according to the New York times.

But what these results mean for both the amyloid theory of Alzheimer’s disease and more importantly for the patients remains to be seen – and experts are divided.

The conversation: As experts have pointed out, the results are currently being taken at face value in a press release; More precise dates will be published throughout the year.

Eisai and Biogen characterize this 27% relative difference as very important, but how important that is is up for debate. Perhaps most important is whether this slowdown in decline will be felt by patients and their caregivers.

The drug’s effect “is small and would not be considered by many to be a minimally clinically meaningful difference,” Lon Schneider, director of the California Alzheimer’s Disease Center at USC, told the NY Times.

However, Schneider concedes that “others would strongly disagree and say it’s clinically meaningful,” he told the NY Times.

The drug may also be most effective in the early stages, which is where the study patients were. “I’m cautiously optimistic that it could potentially be of concern to those who are in the mild stage,” said Mia Yang, a Wake Forest STAT geriatrician.

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