Lecanemab: a breakthrough dementia treatment to slow cognitive decline

Dementia has proved a difficult disease to fully understand. Our knowledge of the disease has grown considerably thanks to research over the past 100 years, but up until this year, no effective treatment had been found.

However, a new antibody drug called Lecanemab may change all that. According to a paper presented at the annual Clinical Trials on Alzheimer’s Disease in San Fransisco, the new drug has been shown to slow cognitive decline in patients diagnosed in the early stages of dementia.

A clinically meaningful impact

The new treatment has been developed by Eisai, a Japanese pharmaceutical firm, and Biogen, a US biotech. In a September press release, the company said that the new treatment had “A clinically meaningful impact on cognition and function”.

What was presented at the San Fransisco meeting at the end of November were the more detailed study results. The team also published a paper in the New England Journal of Medicine, concluding that:

“Lecanemab reduced markers of amyloid in early Alzheimer’s disease and resulted in moderately less decline on measures of cognition and function.”

It’s important to note the word “moderately”. The new drug is a start, an indiction that researchers are on the right track.

As the The University of Rochester Medical Center (URMC) Alzheimer’s Disease Care, Research and Education Program explains:

“This provides the first definitive evidence that clearing amyloid beta improves cognitive performance. It is important to note that both groups experienced cognitive decline over the 18 months of the study, but the placebo group declined at a faster rate.”

A note of caution

The Center also sounds a note of caution:

“(Alzheimer’s) is a disease that will ultimately require combination treatments like some of the resistant cancers, or resistant high blood pressure, or diabetes. Those of us who have been studying Alzheimer’s for a long time have become humble and we recognize that lecanemab is a start and not a cure. It is a modest start, but represents an approach to treatment that we can build upon.”

What is amyloid?

Amyloid is a protein that accumulates in the brain, forming clumps known as plaques. As the News Medical website explains:

“Amyloid plaques are aggregates of misfolded proteins that form in the spaces between nerve cells. These abnormally configured proteins are thought to play a central role in Alzheimer’s disease. The amyloid plaques first develop in the areas of the brain concerned with memory and other cognitive functions.”

How does Lecanemab work?

As Dr Susan Kohlhaas, Director of Research at Alzheimer’s Research UK, said:

“Lecanemab works by clearing the amyloid protein that builds up in the brain in people with Alzheimer’s disease. In this trial, the drug slowed down participants’ decline in memory and thinking, and their ability to carry out day-to-day activities. Although the benefits were small and came with significant side effects, it marks the arrival of a treatment that can slow the course of Alzheimer’s disease.”

It’s been 30 years since the central role played by amyloid protein in the onset of Alzheimer’s disease and dementia, and it has take this long to come up with a single drug that has measurable success. Just like the famous moon landing speech, it might be said to be “Only a first step on the journey towards a cure” (but in time, it could be the giant leap forward overall that scientists have been searching for.

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