Introducing Another Alzheimer’s Drug – A Right Answer To The Wrong Problem?

Last Thursday (6th of July 2023), the FDA fully approved lecanemab (brand name Leqembi) for the treatment of Alzheimer’s disease. Lecanemab doesn’t cure or reverse Alzheimer’s, but it does seem to slow down the progression of the disease if (and it’s a big if) the condition can be detected early enough.

Lecanemab is a monoclonal antibody that works by targeting amyloid beta proteins and preventing their deposition in amyloid plaques within the brain. It was once thought that amyloid beta was primarily responsible for the development of Alzheimer’s disease, but many scientists now believe this theory to be flawed. Amyloid may still play a role in Alzheimer’s disease. However, many suspect that age related changes in the brain, such as increased inflammation and dysfunctional immune cells, are primary causes that may represent more effective targets.

In clinical trials, lecanemab slowed early Alzheimer’s progression slightly when compared to placebo when two infusions were given per week. However, it comes at a high price – $26 500 per year to be precise. Patients on lecanemab were also twice as likely to suffer brain haemorrhaging or swelling as those on placebo, meaning recipients will need careful monitoring.

To further highlight the problems with amyloid beta as a target, it is not as prominent a component of Alzheimer’s disease in all groups. African Americans are twice as likely to develop Alzheimer’s disease as caucasians, but are less likely to have elevated levels of amyloid beta – a condition that is necessary for lecanemab to be useful. They may also be more at risk of haemorrhaging as a side effect of the treatment.

We may not know exactly what causes Alzheimer’s disease, but we do know that regardless of race, gender or environment, the single strongest risk factor for Alzheimer’s is age. If a cure for Alzheimer’s disease is to be found, it is most likely to be rooted in the biology of ageing.