Ten months ago, UCL's Professor Sir John Hardy hailed the Lecanemab trial as the "beginning of the end" for Alzheimer's disease, but this was just the start of a series of exciting developments - with UCL experts at the forefront.
It is estimated that there are currently 944,000 people living with dementia in the UK and 52% of the UK public - 34.5 million - know someone who has been diagnosed with a form of the disease. Over 60% of people living with the condition are thought to have Alzheimer's disease.
Dementia is the nation's biggest killer and has been the leading cause of death in women since 2011. However, there is currently no cure.
UCL is determined to tackle this growing crisis with one of the world's largest neuroscience communities, access to a patient population of more than six million and the construction of a new neuroscience facility at 256 Grays Inn Road, enabled by a visionary community of partners and philanthropic funders.
And, over the past year, the work of the university's talented researchers and clinicians has helped see the success of trials involving drugs such as Lecanemab and ALN-APP - showing that it is possible to slow the rate of cognitive decline in people with Alzheimer's disease and giving hope to millions across the globe.
YouTube Widget Placeholderhttps://youtu.be/_KBYdzFS_OA
Where it started
The results of the Lecanemab trial were published in November last year. It was found to slow down progression and reduce memory decline by targeting beta amyloid - a plaque that builds up in the brains of people with Alzheimer's disease.
Professor Sir John Hardy (UCL Queen Square Institute of Neurology) was the first to identify the role of amyloid in Alzheimer's disease 30 years ago, after he began working with Carol Jennings and her family.
Carol reached out to Professor Hardy and Professor Martin Rossor (UCL Queen Square Institute of Neurology) in the mid-1980s, after her father, his sister and brother, all developed symptoms and were diagnosed with Alzheimer's in their 50s.
Intrigued, Professor Hardy embarked on research to determine whether there were any genetic differences between those who had Alzheimer's and those who didn't.
And, five years later, his team discovered a mutation to the amyloid precursor protein (APP) gene, which creates the amyloid plaques that form in the brain during Alzheimer's disease - causing them to become overactive and signalling for ongoing inflammation, which can disrupt normal processes in the brain.
As a result of the findings, in 1992, Professor Hardy and his colleague, Professor David Allsop, published the amyloid cascade hypothesis, which helped explain:
- The brain appearing smaller due to the death of brain cells
- The build-up of amyloid protein
- Tangles with tau (a toxic protein that causes neuronal death)
