WORLD VIEW
Finding a cure for Alzheimer’s disease, the most common form of dementia, is the Holy Grail of medical research. The incurable malady is — along with other dementias — the leading cause of death in the U.K. Until now, no therapy had emerged that could even slow its lethal brain shrinkage, let alone stop or reverse its grim progression. Treating dementia has also been an underfunded cause. By some estimates, more research has been done on COVID in the past three years than on dementia in the past century. Yet, a drug that works for Alzheimer’s has appeared on the horizon, raising hopes that there may be some relief from a deadly and cruel condition.
The drug, lecanemab, is a landmark in medicine, and the first treatment to slow cognitive decline in Alzheimer’s patients. People understandably focus on breakthroughs that deliver a cure. Dementia is a frightening disease. It may begin innocuously enough, with a little forgetfulness. But the sickness gnaws away at a person’s mental agility, their memory and ultimately their personality. Patients can end up delusional, incontinent and incapable of looking after themselves. Death arrives on average about eight years after the initial diagnosis. Lecanemab’s effect is modest. In a clinical trial involving 1,800 patients in the early stages of Alzheimer’s, the drug slowed its development over 18 months by about a quarter.
Some scientists say that while the results are statistically significant, individual patients might not perceive much — if any — difference. Others have questioned whether the drug’s side-effects outweigh its benefits. The drug, significantly, points to a possible cause of the illness. The theory is that a protein, beta amyloid, and another it encourages, called tau, harm brain neurons to such an extent that they die off. Because lecanemab is an antibody therapy that removes beta amyloid, it provides a much-needed fillip for the hypothesis that the protein might be a key that could unlock Alzheimer’s secrets.
This is no academic discussion. Between 2007 and 2019, more than a dozen final-stage trials of amyloid-targeting drugs reported results. None slowed cognitive decline; some even made it worse. When, last year, a therapy that targeted beta amyloid became the first new Alzheimer’s drug in two decades to receive U.S. approval, because it might help moderate symptoms, the decision became a flashpoint in a vexed scientific debate.
U.S. regulators are expected to approve lecanemab for use in January. Britons will have to wait longer. First, U.K. medical watchdogs would have to judge the drug’s safety, and then if its cost could be justified. If the benefits of lecanemab could be sustained, experts suggest, a patient might have seven and a half years of independent living — rather than the current six — before they need support at home. The arrival of dementia treatments will need more NHS resources. Hospitals would require accurate diagnostic tests to swiftly identify patients likely to benefit, specialist staff to provide regular drug infusions, and MRI scans to keep tabs on patient progress.
Dementia becomes more common in old age. As life expectancy rises, the number of people suffering with the illness will surge. This recent scientific advance is good news. Yet patients will still need to be cared for, often for many years. Dementia is perhaps the greatest medical and ethical challenge of the age. One can only hope that the British state, after a decade of ministers failing to fix the broken social care sector, is up to the test.
The Guardian
