A glimmer of hope in treating Alzheimer’s disease
Neuroscientists are celebrating this week’s publication of the firmest evidence so far of a treatment that slows the terrible, inexorable descent into dementia caused by Alzheimer’s disease. Lecanemab, developed jointly by Eisai of Japan and Biogen of the US, reduced the rate of cognitive decline by an average 27 per cent in a clinical trial with 1,800 early-stage patients.
The enthusiastic response of Alzheimer’s experts — who are using terms such as momentous and game-changing — is understandable. For decades researchers have failed to find a way of altering the personality-destroying course of the disease. More than 50mn people worldwide are living with dementia and the number is projected to exceed 150mn by 2050.
The trial is an encouraging demonstration that the disease can be treated by removing beta-amyloid, the gungy protein that gums up the brain as Alzheimer’s progresses. It should inspire an intensified drive to develop drugs that work better than lecanemab and can be prescribed to millions.
Patients and their families should, though, bear in mind its limitations. Lecanemab slows the progression of dementia by a small but significant extent and there are some indications the benefit will become more marked when patients take it for longer than the 18 months of the clinical trial. But it is far from stopping Alzheimer’s in its tracks, let alone curing the condition.
Several other features will hold back widespread adoption. Lecanemab is not taken by mouth but has to be infused into the patient every two weeks. Diagnostic tests — brain scans and/or lumbar punctures — are required to determine eligibility for treatment. And the drug is not a simple chemical but an antibody, expensive to develop and produce. It is likely to cost well above $10,000 a year per person.
To intensify the big efforts pharmaceutical researchers are already making to develop better Alzheimer’s drugs, they will require more funding from the public and private sectors, as well as charities. The 2022 pipeline has 119 medicines in clinical trials that are designed to slow or reverse the underlying process of neurodegeneration.
The success of lecanemab’s clinical trial ought to encourage other projects to remove amyloid deposits from the brain. There is huge scope, too, for exploring quite different mechanisms that might work well on their own or in combination with anti-amyloid drugs. These include removing tau (another toxic protein associated with Alzheimer’s), reducing cerebral inflammation and enhancing the brain’s capacity to flush out harmful molecules.
Most Alzheimer’s drug candidates are not discovered by pharmaceutical companies but in academic labs and biotech businesses. Lecanemab originated with BioArctic, a small Swedish company that collaborated with Eisai and then Biogen to take it through clinical trials.
A healthy flow of future drugs that could make a real impact on Alzheimer’s and other forms of dementia will depend on nourishing the scientific roots of research and then helping promising projects across the “valley of death” from the labs where they begin life to larger drugs groups whose medical, marketing and manufacturing muscle can guide them through the regulatory process and into patients. More initiatives like the Dementia Discovery Fund, a public-private partnership based in the UK, are needed.
Lecanemab may indeed become a game-changer — but the world needs to invest enough not only in the R&D pipeline but also in building up a broad-based infrastructure of dementia diagnostics and treatment facilities. An ageing global population makes the economic case for this. The reward will be healthier brains for hundreds of millions in decades to come.