Our research strategy

Our focus is to accelerate the ‘bench-to-bedside’ journey: our funding seeks to translate scientific findings into patient benefit as rapidly as possible. 

We fund the very best biomedical research, from basic to clinical, that improves our understanding of all the causes of different dementias or improves diagnosis, prevention and treatment. Social or carer-focussed research is off-remit. Our ultimate goal is a preventative treatment or intervention for neurodegenerative diseases.

We have built a reputation as a flexible and responsive funder, committed to supporting the best and most innovative ideas from across the field. We encourage applications that: address fundamental gaps in our knowledge of disease processes; have a translational path or vision and are collaborative and transparent; ensuring reagents and data are shared with the scientific community.

Our funding is directed towards both translating scientific discovery into patient benefit and in growing the research base. A significant proportion of our funding is allocated towards response-mode applications. While we provide guidance on areas of basic science that are of particular interest, we will fund the best research that takes us towards defeating dementia and we encourage radical new approaches and thinking that change paradigms. Alzheimer’s Research UK’s current basic science priority areas are:

  1. Tau pathology
  • Research into the mechanisms that lead to abnormally folded tau
  • Research into tau pathology transmission
  • Research into tau biomarkers, especially into PET ligands for human use.
  1. Neuronal death
  • Research into mechanisms of neuronal death in neurodegeneration, including in vivo models that feature neuronal death
  • Research into mechanisms that may operate in multiple diseases: e.g. the unfolded protein response; autophagy; ubiquitin proteasome system; chaperones; mitochondrial dysfunction.
  1. ‘Prion’-hypothesis
  • Research into the mechanism underpinning the transmission of pathological protein conformers (e.g., for Aβ, tau, α-synuclein, huntingtin, prion).
  1. Biological and systems deconvolution of genetic risk
  • Models that seek to elucidate the pathophysiology mediated by risk alleles identified from linkage and GWAS.
  1. Aβ pathology
  • Initial seeding of Aβ in brain parenchyma
  • Research into the links between Aβ and tau pathology.

Other areas that are not directly covered in the priority areas, but that nevertheless are of great interest, include:

  • Investigating differences between sensitive and resistant neuronal populations (why is the cerebellum largely spared); neuroprotection and neuro-resilience
  • Neuropathological examination of brains from patients that have been in phase 3 clinical trials of putative disease-modifying therapies
  • Ground-breaking technological advancements that are of particular relevance to the field, e.g. the use of iPS cells to model more accurately human physiology of disease
  • Next generation sequencing to identify rare mutations that have large effect sizes.

We have also identified some areas which are a lower priority for funding:

  • APP trafficking
  • direct toxicity of Aβ in cell culture experiments
  • oligomers and intracellular Aβ (unless combined with unequivocal quantitative measurement)
  • experiments using supra-physiological concentrations of Aβ
  • anti-aggregation approaches (unless there is unequivocal in vivo data for efficacy).

Applications that are focussed on target validation and drug discovery should be directed to ARUK’s Dementia Consortium. Applications that seek to test clinical agents or other interventions should be directed towards ARUK’s Global Clinical Trials Fund.