The Brain Research UK Miriam Marks Research Fellowship scheme was established in 2020 in partnership with UCL Queen Square Institute of Neurology. The scheme is funded by the Miriam Marks Endowment Fund, which was established by the family of Mrs Miriam Marks in 1971 to support research into brain degeneration.
This award to Dr Robert Ellingford is one of two Fellowships awarded in 2026, and will support his research into Alzheimer’s Disease.
Robert is currently a post-doc in the UK Dementia Research Institute at UCL, having completed his PhD at King’s College London in 2020.
During his PhD, Robert investigated early synaptic development in models of autism spectrum disorder, developing expertise in electrophysiology and circuit neuroscience while producing multiple first-author publications. Following this, he joined the UK Dementia Research Institute at UCL as a Postdoctoral Research Fellow in the laboratory of Professor Marc Busche, where he has led projects investigating the early neuronal and network dysfunction underlying Alzheimer’s Disease.
This Miriam Marks Fellowship will enable Robert to pursue this line of research under the continued supervision of Professor Marc Busche. It will also provide the ideal platform to enable Robert to establish his own independent research direction while developing the leadership, collaborative, and technical skills required to build a future research group focused on neuronal dysfunction in neurodegenerative disease.
Alzheimer’s Disease is the most common cause of dementia.
Increasing age is the greatest risk factor for Alzheimer’s, with the risk of developing the disease doubling every five years beyond the age of 65 years.
Genetic factors also play an important role in Alzheimer’s risk, conferring as much as 60-70% of the risk of developing the disease in old-age. Whilst the vast majority of cases are not directly inherited, there are around 20 genes that are known to be associated with the disease. A number of ‘life course’ risks (such as hypertension and diabetes) have also been identified. How and why these life course and genetic risks combine to lead to the initiation and evolution of Alzheimer’s is not yet known.
The pathological changes underpinning Alzheimer’s are thought to develop at least a decade prior to the onset of symptoms, giving a window of opportunity to not only track the evolution of the disease but also potentially to intervene to prevent the onset of cognitive symptoms.
Read more: Alzheimer's Disease and dementia
The hallmarks of Alzheimer’s Disease are extracellular amyloid plaques – deposits of amyloid beta (Aβ) protein that present mainly in the grey matter of the brain – and intracellular tau aggregates – clumps of tau protein that form within brain cells.
Although recent therapies targeting Aβ can modestly slow cognitive decline, they do not halt disease progression, highlighting the need for deeper mechanistic insight into how certain proteins drive neuronal dysfunction and degeneration.
This fellowship is aimed at understanding how Aβ and tau work together to disrupt the normal activity of neurons in Alzheimer’s Disease. The central hypothesis is that Aβ and tau interact to impair normal neuronal activity through distinct mechanisms that cannot be explained by either Aβ or tau alone.
The project combines human brain tissue work, advanced imaging and electrophysiological techniques, and in vivo studies to (1) define how Aβ and tau alter neuron and network function both independently and in combination, and (2) determine whether the processes identified in (1) can be therapeutically targeted to restore neuronal function and improve cognition.
Alzheimer’s Disease affects more than 50 million people worldwide and accounts for approximately 60-80% of dementia cases. Despite major advances in our understanding of the disease, Alzheimer’s Disease remains incurable and places enormous emotional and economic burdens on patients, families, and healthcare systems.
By establishing a translational experimental platform using human brain tissue alongside validated Alzheimer’s Disease models, this project will identify mechanistic drivers of neuronal dysfunction and uncover novel therapeutic targets for treating Alzheimer’s Disease.
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