FFinding a cure for Alzheimer’s disease, the most common form of dementia, is the holy grail of medical research. The incurable disease is, along with other dementias, the main cause of death in the UK. Until now, no therapy had emerged that could slow her lethal brain shrinkage, let alone halt or reverse her grim progression. Dementia treatment has also been an underfunded cause. By some estimates, more research has been done on covid in the last three years than on dementia in the last century. However, this week, a drug that works for Alzheimer’s has appeared on the horizon, raising hopes that there may be some relief from a cruel and deadly condition.
The drug, lecanemab, is a milestone in medicine and the first treatment to delay cognitive decline in Alzheimer’s patients. People understandably focus on breakthroughs that provide a cure. Dementia is a scary disease. It can start innocuously enough, with a bit of forgetfulness. But the disease eats away at a person’s mental agility, their memory and, ultimately, their personality. Patients may end up delirious, incontinent, and unable to care for themselves. Death comes on average about eight years after the initial diagnosis. The effect of lecanemab is modest. In a clinical trial involving 1,800 patients in the early stages of Alzheimer’s disease, the drug delayed its development by 18 months by about a quarter.
Some scientists say that while the results are statistically significant, individual patients may not perceive much of a difference, if at all. others have disputed if the side effects of the drug outweigh its benefits. The drug, significantly, aims at a possible cause of the disease The theory is that a protein, beta amyloid, and another that it stimulates, called tau, damage brain neurons to such an extent that they die. Because lecanemab is an antibody therapy that removes beta amyloid, it provides a much-needed boost to the hypothesis that the protein could be a key that could unlock the secrets of Alzheimer’s disease.
This is not an academic discussion. Between 2007 and 2019, more than a dozen end-stage trials of drugs targeting amyloid reported results. None slowed cognitive decline; some even made it worse. When, last year, a beta-amyloid-targeted therapy became the first new Alzheimer’s drug to receive U.S. approval in two decades because it could help moderate symptoms, the decision became a Flash point in a controversial scientific debate.
US regulators are expected to approve the use of lecanemab in January. The British will have to wait longer. First, UK medical watchdogs would have to judge the drug’s safety and then whether its cost could be justified. If the benefits of lecanemab could be sustained, experts suggest, a patient can have seven and a half years of independent living, instead of the current six, before needing support at home. The advent of dementia treatments will require more NHS resources. Hospitals would require accurate diagnostic tests to quickly identify patients who might benefit, specialized staff to provide regular infusions of drugs, and MRIs to monitor patient progress.
Dementia becomes more common in old age. What increases life expectancy, the number of people suffering from the disease will increase. This week’s scientific breakthrough is good news. However, patients will continue to need care, often for many years. Dementia is perhaps the greatest medical and ethical challenge of the time. One can only hope that the British state, after a decade of ministers failing to fix the bankrupt welfare sector, will rise to the test.
