Dementia Support Line
2022/23 Cohort of Dementia Research Leaders
In our 2022/23 grant round, we funded seven exceptional dementia researchers to become our next Dementia Research Leaders. Read more about their research and motivations.
Dr Hugo Fernandes
Can changes in fat and cholesterol drive dementia?
Dr Fernandes has built an international research career, graduating from the University of Minho in Portugal, undertaking research training in the Netherlands and Sweden, and completing a PhD at the University of Oxford. He later worked at the Sanger Institute and the UK Dementia Research Institute at the University of Cambridge before returning to Oxford.
My project will seek to advance our understanding of the causes of dementia and to provide better treatment options to improve patients' quality of life.
Dr Chris Henstridge
Investigating the processes behind TDP-43 protein in dementia
Dr Chris Henstridge at the University of Dundee began researching dementia through his fascination with the brain. After several family members were diagnosed with different forms of dementia, he became determined to understand the underlying brain changes. In 2019, he established his own research group at Dundee, which has made important discoveries in Alzheimer’s disease, frontotemporal dementia and motor neuron disease.
Research is our route to treatment. With five years of funding, I can now implement more ambitious research plans and, importantly, hire new young researchers to help direct it.
People living with Alzheimer’s disease, Frontotemporal dementia, or Amyotrophic Lateral Sclerosis (ALS; the most common form of Motor Neuron Disease) all show different symptoms on the outside - but inside the brain, some changes can look very similar.
For example, in all three diseases, the connections between brain cells – called synapses – start to break down. Another big change is that certain proteins stick together in unusual clumps, which stop brain cells from working properly. One of the proteins that clumps in all three diseases is called TDP-43.
These changes suggest similar processes may be happening in brains of people with these different diseases.
Dr Henstridge hopes that by understanding what happens to TDP-43 and synapses in one type of dementia, we could learn more about what happens in other types. Through his research, he aims to:
- investigate how synapses change in disease
- discover what TDP-43 does at the synapse
- see if synapse breakdown can be used as an early warning signal of disease.
Dr Chris Henstridge said,
'Funding for dementia research is not where it needs to be. Your donations have, and will continue to have, a huge impact on what we do and for that we, the researchers, are very grateful.'
Dr Johanna Jackson
How are brain connections lost in dementia?
Dr Johanna Jackson is an Advanced Research Fellow, the first recipient of the Alzheimer's Society's Carol Jennings Fellowship and a UK DRI Emerging Leader at the UK Dementia Research Institute at Imperial College London. Dr Jackson now leads a research team at Imperial College London, working to understand synapses and how they are affected in disease.
The Society recognised the diverse skills I developed in industry and academia and how they could support Alzheimer’s disease research, particularly in addressing problems with brain cell communication.
Brain cells communicate through small connections known as synapses. In Alzheimer’s disease, these connections become damaged or lost, which is closely linked to symptoms like memory loss and confusion.
Synapses have two parts: one that sends signals and one that receives them. Both rely on specific proteins to function properly, but in Alzheimer’s, this system breaks down.
Dr Jackson’s work aims to understand exactly how and why these proteins are lost, by studying the biological ‘blueprints’ (RNA) that create them.
She will also look at whether an existing epilepsy drug, known to affect synapses, could help restore damaged ones in the brain. This research could open the door to new treatments that protect or repair these vital connections in Alzheimer’s disease.
Dr Johanna Jackson said,
'I find inspiration in dementia research that is translational in nature, by gaining an understanding of basic mechanism whilst seeking to identify targets to change the course of the disease.'
Dr Leeanne McGurk
How is protein build-up controlled and how does it lead to dementia?
Dr McGurk was motivated to become a dementia researcher during her PhD, while studying brains of fruit flies. Through this work, she discovered that the fruit fly brain could be a powerful model for exploring and understanding the basic mechanisms of dementia. Today Leeanne leads a research group investigating how protein build-up leads to dementia at the University of Dundee.
Discovering how the two proteins Tankyrase and TDP-43 interact will make a huge difference to our understanding of dementia and will be a gateway to new medicines.
The protein TDP-43 plays an important role in dementia. In a healthy cell, this protein stays in its usual place and supports normal function. In dementia, however, it becomes displaced and builds up in another area, where it harms the cell. This TDP-43 build-up is common in dementia - in 45% of people with frontotemporal dementia and 57% of people with Alzheimer’s disease.
Dr McGurk’s research showed that another protein, Tankyrase, can stick to TDP-43 and speeds up its harmful build-up. Her research also found that when Tankyrase is reduced or blocked, it stops TDP-43 from damaging the cells.
Currently, Dr Leeanne McGurk’s research aims to find out how Tankyrase sticks to TDP-43, and how it controls its build-up.
Dr McGurk said,
'The Alzheimer’s Society Dementia Research Leaders Fellowship has been vital to me as it has enabled me to start a lab, build a team, develop a research program, and develop the careers of people who have joined the research team.'
Dr Sarah Ryan
Can we target the brain’s immune system as a potential therapy for frontotemporal dementia (FTD)?
Dr Sarah Ryan has over a decade of experience researching dementia at the University of Manchester. Since 2019, she has been supported by Alzheimer’s Society. Her first grant, a Junior Research Fellowship, investigated the causes of frontotemporal dementia, and the DRL Fellowship now enables her to continue this work and improve understanding of this complex condition.
If this research is successful, we may be able to re-purpose existing drugs to treat FTD. Through my work, I hope to provide the research community with vital new insights into the role of microglia in disease.
Frontotemporal dementia (FTD) is the second most common type of dementia affecting younger people and there are no treatments currently available.
Our brains have their own special immune cells, called microglia. You can think of them as the brain’s clean-up crew, they fight infection and clear away waste. But in FTD, these clean-up cells can become overactive, which leads to them harming the brain.
Dr Ryan and her team will use a mouse model of FTD which mimics the brain environment of people with the most common form of FTD. By using genetic tools and potential drug treatments, Dr Ryan will try to prevent microglia from becoming overactive, reducing the damage they cause to the brain.
Dr Ryan’s goal is to investigate several drugs which are already available for other conditions, to see whether they would be helpful in treating FTD.
She will also investigate the complex mechanisms which activate microglia in the brain, to understand the processes that cause FTD.
Dr Sarah Ryan said,
'The support from Alzheimer’s Society has been a key part of my career, giving me the confidence and stability to continue pursuing my research and make meaningful progress in understanding frontotemporal dementia.'
Dr Kamen Tsvetanov
Understanding brain resilience and how the brain adapts to change
For Dr Kamen Tsvetanov, at the University of Cambridge, dementia research is like solving a complex puzzle. It takes many different perspectives to see a full picture. A senior researcher in cognitive neuroscience of ageing and dementia, his work focuses on brain resilience.
This fellowship isn’t just about funding; it’s personal. It’s like having the voices of people affected by dementia and everyone who supports the Society with me on this research journey. Every brain scan, every data point, and every discovery brings us closer to a world where dementia can be prevented.
We know that brain changes can begin many years before the symptoms of dementia appear. Our brains are good at resisting damage from disease, but over time this natural resilience is worn down. Increasing brain resilience could help to prevent dementia and protect brain health as we get older.
Dr Tsvetanov’s research tries to find out why some people’s brains stay healthy even when they have a disease, and what causes dementia symptoms to finally show up.
He hopes that understanding brain resilience will open treatment strategies in three ways:
- Identifying people at risk of dementia, despite not having symptoms, such as memory loss.
- Helping clinical trials test new interventions more effectively.
- Shifting research to focus more on brain health over time.
Dr Kamen Tsvetanov explains his approach:
'I use new ways to examine brain scans across all ages. I assess when the brain starts to lose tissue and when different parts of the brain stop 'talking' to each other.
This research represents a fundamental shift from managing dementia to preventing it entirely. By understanding what keeps brains resilient, we're not just studying the disease—we're learning how to stop it.'
Dr Ryan West
How does the loss of protein building blocks link to frontotemporal dementia?
Dr Ryan West’s dementia research career has been supported by Alzheimer’s Society from the start. His PhD funding enabled him to gain real-life insights from our Research Network Volunteers. He is now a Senior Fellow at the University of Sheffield, leading a group studying the mechanisms underlying frontotemporal dementia (FTD).
I’m committed to my research because I enjoy it and because, hopefully, my research is making a difference.
Frontotemporal dementia (FTD) is the second most common form of early-onset dementia. The most common genetic cause of FTD is a mutation in a gene called C9orf72. The symptoms and age of onset can vary a lot between people and researchers don’t yet fully understand why.
Dr West’s project uses fruit flies and cell models to study five toxic proteins produced by this mutation. These proteins behave differently depending on which brain cells they’re in and whether they act alone or together.
By studying how and where these toxic proteins cause damage, Ryan’s team hopes to better understand why FTD symptoms vary between people. This could lead to more targeted and effective treatments in the future.
Dr Ryan West said,
'Being awarded my Alzheimer’s Society fellowship represented a real stepping stone between being a post-doctoral researcher and starting to set up my own, fully independent research lab.'
Our research
Today, Alzheimer's Society is supporting world-leading dementia research with over £50 million in investment. Our funded research will bring breakthroughs in how we understand the causes of dementia, develop effective treatments, improve care and ultimately find a cure for dementia.
Fats are essential molecules in the human body with multiple cellular functions. Remarkably, fats represent over 50% of the adult human brain. Yet, very little is known about their role in brain cells in dementia.
Dr Fernandes recently discovered that changes in specific fats, known as cholesterol, in human nerve cells are associated with the loss of brain cells. He suggests that fats could be key drivers of dementia.
Research aims:
This research could provide new targets for early diagnosis, disease intervention and treatments.