People suffering from the most common type of dementia, Alzheimer’s, might soon get a revolutionary drug for the disease

Individuals who have difficulty performing daily tasks due to Alzheimer’s, which is the most common cause of dementia, could be finally relieved as a new revolutionary cure for the disease is in sight.

A leading specialist in this area said patients might be able to receive the treatment as soon as next year, but has also warned dementia services that they have a lot of work to do in order to provide the medicine in the event that it receives regulatory approval.

During clinical tests, the medication known as Lecanemab was capable of clearing the brain of harmful amyloid protein and delaying the development of symptoms, making it the first medicine in the world aimed at preventing slow brain decline.

A top geneticist, Professor Sir John Hardy, said he was confident a new era of treatments targeting amyloid was on the horizon.

Speaking at an event hosted by the Science Media Centre, Sir John said, “I’m really excited about the work that’s going to be presented because we’ve seen press releases and that’s a little bit dangerous.”

“I actually think this is a historic moment.” “It’s taken a long time to get here, and we first suggested amyloid therapies in 1992.”

The monoclonal antibody treatment showed promise in a Phase 3 trial, the results of which were published in September.

The immunotherapy drug was tested in a study of 1,795 patients with early-stage Alzheimer’s disease in the US, Japan, Europe, and China.

Results showed it reduced the rate of cognitive decline by 27 percent after 18 months compared to a placebo, according to its manufacturers, Tokyo-based Eisa and US firm Biogen.

These effects were measured using a scale that assessed several cognitive domains: memory, orientation, judgement, problem solving, community affairs, home, hobbies, and personal care.

One side effect observed during the study was brain swelling, at a rate of 12.5 percent for patients on Lecanemab, compared to 1.7 percent in the placebo group.

The companies, however, noted that such aftereffects are “within expectations.”

The full data of the trial is due to be presented at a major Alzheimer’s conference on November 29 and published this year in a peer-reviewed journal.

Scientists hailed the discovery as a key milestone in the ongoing battle to beat dementia.

Although it is not a cure, it may help prolong the quality of life of millions of patients currently afflicted by neurodegenerative diseases.

Speaking at a briefing ahead of the conference, Doctor Susan Kohlaas, director of research at Alzheimer’s Research UK, said: “The Lecanemab results bring a renewed sense of urgency to really improve the way we diagnose diseases like Alzheimer’s disease.”

Doctor Liz Coulthard, associate professor in dementia neurology at the University of Bristol and North Bristol NHS Trust, noted: “Over the years we have, as a profession, not used the biochemical definition of Alzheimer’s because we’ve not been able to test for it until after people have died.”

“But we’ve now got biomarker tests that have come into the clinical sphere in the last five years or so that we can actually diagnose people accurately with Alzheimer’s disease.”