The first drug to slow brain destruction in Alzheimer’s has been hailed as a breakthrough.
A research breakthrough ends decades of failure and shows a new era of drugs to treat Alzheimer’s – the most common form of dementia – is possible.
Yet the drug, lecanemab, has only a small effect and its impact on people’s daily lives is debated.
And the drug works in the early stages of the disease, so most will miss it without a revolution in detection.
Lecanemab attacks the sticky plaque – called beta amyloid – that builds up in the brains of people with Alzheimer’s.
For a medical field filled with despair, hopelessness and despair, some see these trial results as a triumphant turn.
Alzheimer’s Research UK said the findings were “surprising”.
Professor John Hardy, one of the world’s leading researchers behind the whole idea of ​​targeting amyloid 30 years ago, said it was “historic” and was optimistic that “we are seeing the beginning of a cure for Alzheimer’s”. Professor Tara Spiers-Jones, from the University of Edinburgh, said the findings were “a big deal because we’ve had a 100 per cent failure rate for a long time”.
Currently, people with Alzheimer’s are given other drugs to help manage their symptoms, but none reverse the course of the disease.
Lecanemab is an antibody – like the one the body makes to attack a virus or bacteria – that is designed to help the immune system clear amyloid from the brain.
Amyloid is a protein that accumulates in the spaces between neurons in the brain and forms the characteristic plaques that are one of the symptoms of Alzheimer’s.
