Alzheimer’s Research UK Conference 2018: Day 2

Written by Rebecca MC Gabriele (Kings College London, UK)

Aging is inevitable but dementia is not. The Alzheimer’s Research UK (ARUK) manifesto, “the power to defeat dementia,” is not just a state motto, it is a goal. Through research, this mission can become a promising reality.

Read our conference report from Day 1 here

Energy metabolism, aging and neurodegeneration

The second and final day of the ARUK Conference 2018 (London, UK) was opened by Grahame Hardie from the University of Dundee (UK). Hardie presented a great talk on AMPK, its crucial role in regulating cell energy homeostasis and its potential target for drug treatment. The stage was then taken by Jill Fowler, ARUK Senior Research Fellow from the University of Edinburgh (UK). Fowler brilliantly illustrated how, following cerebral hypoperfusion, upregulation of the neuronal factor Nrf2 can prevent white matter damage and protect from cognitive impairment. This is even more interesting if one considers that cardiovascular conditions increase the likelihood of developing dementia. Helene Puln-Favreu from University College London (UCL; UK) closed the session with a beautiful talk on mitophagy in neurons and how targeting this cellular mechanism may be a possible therapeutic approach for neurodegenerative disease.

A coffee break and poster presentation followed the first session, which gave conference attendees and guest speakers not only the opportunity to exchange ideas but to observe the fascinating ongoing research through poster sessions and networking.

Insights from other dementias and diseases

It is worth mentioning that dementia is not a synonymy for Alzheimer’s and in fact, the second session of the conference focused on other types of dementia and diseases. The first speaker was Karen Horsburg (University of Edinburgh), who discussed microglia alteration following hypoperfusion. A better understanding of how microglia react following reduction of blood flow may help elucidate neurodegenerative disease progression. The session continued with Dag Aarsland from King’s College London (KCL) presenting his talk on dementia with Lewy bodies (LBD). Although LBD represents a very common form of dementia, available tools to study the disease are meagre and the state of research is behind. Aarsland brought up the necessity to do more in the future to better understand LBD.  Following, Sarah Mizielinska (KCL) presented a remarkable study on dipeptide protein repeats (DRP). Mizielinska’s research focuses on the effects of DPR nuclear pore in frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS). The fourth talk of the session was delivered by Jane Armitage from Oxford University (UK) with a discussion on whether treatment of vascular risk factors can have a positive effect on cognitive decline due to aging. The session was concluded by PhD student Richard Hale (University of Salford, UK) who spoke about autophagy aberration in FTD. It was inspiring to see such a young researcher taking the stage.

All things tau

Following the lunch break, which was another fabulous opportunity to visit more posters and discuss research with other attendees, the conference continued with a session focused on tauopathies. Ben Falcon (MRC Laboratory of Molecular Biology, Cambridge, UK) inaugurated this session with a brilliant talk on the structural differences of tau within the same disease and between diseases. Falcon applied electron cryo-microscopy to study the protein structure, which led to astonishing results. The session continued with Diane Hanger (KCL) who delivered an interesting talk on the Tau35 fragment. Hanger’s lab generated animal and cell models to investigate aberrant tau cleavage. Along the same theme, Nigel Hooper from the University of Manchester (UK) illustrated his work on granzyme A as a potential protease involved in tau cleavage, as well as a new potential way to identify novel disease biomarkers.

Prize presentations

Dementia research has made important headways in the past few years and some of the studies that have been conducted need to be acknowledged. Following the third session, ARUK announced winners of two prestigious prizes. Davina Moss, UCL Institute of Neurology (IoN), was awarded the Jean Corse Prize for her most recent publication on Huntington disease [1]. The winner of the David Hague Early Career investigator of the year was Selina Wray (UCL). Wray has been working on induced pluripotent stem cells (iPSCs) and has made important contributions toward the understanding of tauopathies.

Treatments and targets

After a short break, attention shifted toward treatment for dementia in the next session. The first speaker, Patricia Salinas (UCL), talked about her remarkable work on modulation of Wnt signaling as a possible therapeutic strategy for synapse preservation and recovery. Following this, Kurt De Vos (University of Sheffield, UK) illustrated his brilliant work on axonal transport and its impairment in disease. Importantly, De Vos underlined that recovery of axonal transport is possible. Finally, the Chief Scientific Officer of the Cambridge Drug Discovery Institute (UK), John Skidmore, emphasized that targeting proteostasis can be an effective therapeutic strategy to fight neurodegenerative disease. A keyword during this session was ‘recovery’. The idea that we can do something not only motivates the scientific community to carry on the research but I believe it gives some hope to those affected by dementia.

Closing remarks

Before closing the ARUK 2018 Conference, prizes were assigned in recognition of people who were particularly brilliant during the conference. The Dick Bell prize for the best presentation by an early career researcher was awarded to Ben Falcon (MRC Laboratory of Molecular Biology) for his work on tau structure. Yolanda Ohene (UCL) received the David Dawbran poster prize; her poster on non-invasive investigation of waste clearance in the brain was exceptional. Last, James Quinn (University of Manchester) was awarded the Laura Pulford Prize for his interesting talk on tau cleavage at the Early Careers Day.

The conference concluded with ARUK’s CSO David Reynolds, who thanked everyone for making this year’s conference a success. Reynolds emphasized once again the importance of research to defeat dementia and how collaboration is a key component.

The ARUK 2018 Conference was an unforgettable experience that brought together a wide spectrum of expertise. The idea of spacing over other types of dementia was widely appreciated by many as Beatriz Perez Nievas (KCL) stated: “what has emerged is that interdisciplinary approach is essential to find a cure for dementia.” Furthermore, ARUK supports young scientists and this was extremely evident throughout the entire conference. Younger researchers, including myself, enjoyed the emphasis on early career scientists. David Dawbran prize winner Yolanda Ohene described the conference as: “fun and a very educative experience.”

ARUK is doing an incredible job to support the scientific community and improve the lives of many people. I am thrilled to be a part of this fight against dementia and I truly hope that our research will be able to become a tangible solution to dementia.

Read our conference report from Day 1 here


  1. Hensman Moss DJ, Pardinas AF, Langbehn D et al. Identification of genetic variants associated with Huntington’s disease progression: a genome-wide association study. Lancet Neurol., 16(9), 701– 711 (2017).


Biography – Rebecca Maria Cecilia Gabriele

Rebecca began her academic career at Arizona State University (AZ, USA) where she graduated with a degree in Genetics, Cell and Developmental Biology. She then continued her studies at the University of Bologna (Italy) where she obtained a Masters in Molecular and Cellular Biology. During the final year of her master’s she began to develop an interest for neuroscience. Rebecca is now a PhD student at KCL, where she investigates the role of a new genetic risk factor of Alzheimer’s disease, termed BIN1. She is interested in understanding whether BIN1 plays a role in Alzheimer’s disease by modulating the unfolded protein response. 


  1. Neuro Central