Professor Nick Fox is a leading neurologist, specialising in young‑onset and familial dementias. He is Professor of Clinical Neurology and Director of the Dementia Research Centre at UCL’s Queen Square Institute of Neurology, as well as a Group Leader at the UK Dementia Research Institute at UCL. His pioneering MRI methods transformed early detection and tracking of Alzheimer’s disease, enabling pre‑symptomatic measurement of brain changes and accelerating trials of disease‑modifying therapies. Motivated throughout his career by the families he met, Professor Fox is the co-director of Rare Dementia Support, a service for people affected by seven of the rare dementias and is currently spearheading the opening of The Hilary and Galen Weston Rare Dementia Support Centre, the world’s first dedicated centre for rare and early-onset dementias, led by UCL and supported by the National Brain Appeal.
To mark Brain Awareness Week 2026, Professor Nick Fox reflects on his career, including his biggest breakthroughs, proudest moments and what keeps him motivated.
What initially inspired you to work in dementia research and what keeps you motivated?
I didn’t set out to work in neurology at all, and instead I was considering career in public health. However, during a neurology post at Queen Square while I was working as a junior doctor, I found myself inspired by the people I met, both colleagues and patients, and around this time I was encouraged to apply for one of the first Alzheimer’s Society clinical fellowships in MRI methods. My background was in physics and maths, and despite knowing very little about brain imaging, one of the consultants at the National Hospital for Neurology and Neurosurgery suggested that this Fellowship might dovetail my interests quite nicely. I got shortlisted and, despite having probably one of the worst interviews, I was offered the Fellowship!
That’s what got me into dementia research, but what has kept me interested and motivated throughout my career has been the families I’ve met, especially through my work on familial Alzheimer’s disease. These are people who may develop symptoms in their 30s, 40s or 50s and they know there’s a 50% chance of passing it on. Their generosity and courage in contributing to research has been extraordinary. And it is because of their contribution that we’ve challenged the idea that Alzheimer’s arrives suddenly. Their stories, combined with the brain imaging has shown that it’s a slow, subtle process. This has opened the door to understanding early changes in the brain and to trials aiming to intervene before symptoms begin. It continues to motivate me today.
Looking back over your career, what do you consider to be your biggest breakthrough or proudest moment?
Looking back, I think one of my biggest breakthroughs came quite early in my career, during my PhD. I realised that instead of trying to measure one brain scan against another in isolation, the real insight came from looking at change over time. Comparing two brain scans over time is a bit like drawing around your hand twice and trying to see which outline is bigger, a surprisingly difficult task. But what I did was to put the scans on top of each other and subtract the second from the first. Suddenly, the smallest differences became measurable.
That idea became a method, and that method ended up shaping the rest of my career. It allowed us to show that brain changes in Alzheimer’s begin years before symptoms, which opened the field to truly early‑intervention research.
Then, right after my PhD, I was asked if I would use this technique to analyse the brain scans in the world’s first trial for Alzheimer’s disease, which was aiming to try and slow the disease. Hundreds of scans from 50 centres around the world were sent to UCL, and I looked at every single one. An experience and responsibility that was both thrilling and terrifying! Although that early trial had to stop because of side effects, it laid the foundation for what, 25 years later, became the first disease‑modifying therapies for Alzheimer’s. There’s a strange sense of things coming full circle, particularly because the families I first studied had a genetic mutation that causes a build-up in the brain of a protein called beta-amyloid which is what those therapies target.
Then in terms of my proudest moments, more recently, I’ve been part of the team establishing The Hilary and Galen Weston Rare Dementia Support Centre, the world’s first dedicated centre for rare and early-onset dementias, led by UCL and The National Brain Appeal. For years I would diagnose people from all over the UK with young‑onset or inherited dementias, and then they would go home, often to places without any specialist support. So, with colleagues, we built support groups, and eventually, with The National Brain Appeal, took on the enormous task of fundraising for a dedicated centre. People ran marathons, raised money and charitable foundations stepped in. The centre will open later this year, which feels like a real achievement, not just for me but for everyone involved.
As UCL celebrates 200 years of discovery, what past breakthrough in your field inspires you most, and what future breakthrough do you hope to see?
A major breakthrough that inspires me is the discovery of the first gene for Alzheimer’s disease here at UCL. It identified amyloid as the key protein involved, which shaped everything that followed, and it was made possible not just by scientists like John Hardy and Martin Rossor, but by the extraordinary families who took part in that research.
The Jennings family were absolutely central to that breakthrough. Carol Jennings, who I first met when I was a very junior research fellow and whose involvement was pivotal in identifying the gene, was honoured in UCLs bicentenary celebrations. Seeing her recognised was profoundly meaningful and a reminder that progress in dementia research is always a partnership between scientists and families.
Looking ahead, what I hope for in the next five to ten years is the development of therapies that can genuinely prevent this disease from occurring in the first place. We already know from anti‑amyloid therapies that we can slow progression once symptoms begin, and that goes right back to the very first study I worked on. But the real goal, and challenge, is in intervening before symptoms start, when the disease has far less momentum and far less damage has occurred – and there is most to save in terms of brain cells and quality of life.
If we can do that successfully, we’ll see something remarkable: families who for generations have seen members, gene carriers, develop Alzheimer’s in their 30s or 40s, reaching their 40s, 45, even 50, and realising, “I’ve watched my children grow up and I’m still well.” That’s the breakthrough I’d most like to see in the next decade.
What’s the best advice you would give your younger self?
I’d tell my younger self not to be afraid of stepping off the conventional path. Following an unusual route slowed my training slightly, but it opened up opportunities that I would never have had otherwise. I’d also say: find the niche that genuinely motivates you, pursue it even if it isn’t the most traditional option, and remember there’s no rush. Starting medicine later didn’t make any difference in the long run. Research is a long game, and it’s far more important to follow the direction that feels right than to get there quickly.