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Since 2011, Alzheimer’s disease has been the leading cause of death in the UK. There is currently no cure.

Funded by , Dementia Futures offers a valuable opportunity for researchers to network, share knowledge and present key findings about ongoing dementia research to the general public. Held at the ºù«Ӱҵ Institute for Translational Neuroscience (SITraN), the event was filled with engaging talks and discussions by PhD students, postdoctoral researchers and senior researchers working in dementia research.

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Across the institutes at the University of ºù«Ӱҵ we produce a wealth of research within the area of dementia. This event is a great opportunity for us to bring our research to the general public and show them the work that is happening right on their doorstep, as well as hearing the views and opinions of those impacted by the disease. We invited people living with dementia and members of the council to learn how we’re contributing to improving the lives of people with dementia. The event also encouraged our PhD students to improve their communication skills by leaving their labs to showcase their research to the public.

Dr Osman Shabir

Event organiser, BHF Immediate Postdoctoral Fellow and member of the Healthy Lifespan and Neuroscience Institutes

The programme included a presentation from Alzheimer's Research UK by Sara Grix, a discussion on 'can brain connectivity predict risk for developing Alzheimer's risk?' by Giannis Sentris, an undergraduate Bioengineering student at the University of ºù«Ӱҵ and a talk on 'seeing inside the living brain' by Dr Rene Frank from the University of Leeds.

Here’s how members of the Neuroscience and Healthy Lifespan Institutes engaged this year.

Exploring the mechanisms of amyloid beta in Alzheimer’s disease

Dr Emma Garland is a Postdoctoral Researcher at SITraN and member of the Neuroscience Institute. There are two forms of amyloid beta which can clump together in different quantities - one form, amyloid beta 40, is present in higher amounts in the normal bran and is through to be ‘non-toxic’. In Alzheimer’s disease, amyloid beta 42 is increased and it has been reported that this form of the protein is more toxic, which causes some of the issues seen in the disease. Emma’s project will first examine how these two forms of amyloid beta interact and clump together when the amount of each is changed. The research aims to characterise amyloid beta in human tissue and observe how the levels of each form of protein change in disease. The project will also investigate the potential use of the ‘non-toxic’ amyloid beta 40 as a therapeutic to reduce disease issues in models.

Investigation of how amyloid protein clumps interact with astrocyte brain cells in Alzheimer’s disease 

Hollie Wareing is a PhD student at SITraN and member of the Neuroscience Institute. A protein called Amyloid is believed to interfere with how brain nerve cells communicate with each other and cause them to die over time. While nerve cells are the main brain workers, another type of brain cells called astrocytes are essential for the support and protection of nerve cells. One role of astrocytes is to clear the amyloid clumps, however in Alzheimer’s disease this function does not work properly. Hollie’s project created conditions where amyloid clumps together in normal and disease-like ways and observed how the astrocytes cleared these clumps. Astrocytes from healthy and Alzeimer’s patients clear amyloid differently. The results increase our knowledge of the clearance of amyloid by astrocytes, and how it contributes to disease.

Does systematic infection modulate astrocyte function in Alzheimer’s disease?

Zoe Moore is a PhD student at SITraN and member of the Neuroscience Institute. Astrocyte function changes in Alzheimer’s disease, and it is hypothesised that this change could be even more significant when somebody with Alzheimer’s disease gets an infection in their body. Using post-mortem brain tissue and a method called immunohisochemistry, her project aims to detect changes in astrocytes in order to understand how astrocyte function may change in Alzheimer’s disease patients that also have an infection. In the Alzheimer’s disease cases, there was a greater expression of this enzyme in those who died with an infection compared to those without, suggesting astrocytes might adapt to infection in the body and regain some protective function. In the future, Zoe will examine the expression of a more extensive panel of astrocyte markets to build up a bigger picture of what happens in the brains of people living with dementia in response to infection.

Dementia and the basal ganglia 

Harriet Brooke is a PhD student and member of the Neuroscience Institute. Alzheimer’s disease and vascular dementia are the main types of dementia, but in late-life dementia different diseases may be present at the same time. The basal ganglia are composed of several areas deep within the brain, involved with coordination and posture. The basal gangia are often affected by both vascular and Alzheimer’s type pathology, but how this contributes to dementia is not known. 550 brains were donated as part of the Cognitive Function and Ageing Study (CFAS) that looked at dementia in the general population of people over the age of 65. Using various techniques, Harriet’s research is aiming to describe and quantify the different types of damage to small blood vessels and Alzheimer’s-type pathology. The releationship of these different pathologies to dementia will then be examined using statistical methods. So far, initial studies have identified different types of vascular pathology in the basal ganglia and have found that they significantly associate with eachother. 

The effects of heart disease on Alzheimer’s disease

Rahul Sidhu is a PhD student and member of the Healthy Lifespan and Neuroscience Institutes. The brain is an energy-hungry organ and requires a constant supply of oxygen and energy. Fortunately, the brain is nourished by the body’s richest network of blood vessels. Neurovascular coupling is the mechanism that delivers oxygen and nutrients to active regions of the brain. The breakdown of neurovascular coupling has been linked to Alzheimer’s disease. One of the major risk factors for Alzheimer’s disease is atherosclerosis (heart disease). During his PhD project, Rahul has combined a mouse model of Alzheimer’s disease with a model of atherosclerosis to conduct memory tests of mice as well as a post-mortem analysis to see how atherosclerosis affects brains with Alzheimer’s disease. The expected value of this research is to increase the understanding of how, and when, heart disease contributes to the speed, severity and progression of Alzheimer’s disease. By targeting brain blood vessels, we may be able to reduce the risk of developing dementia and slow down the progression of Alzheimer’s disease.

Developing a carer-facing automated assessment tool to track changes in people with dementia

Labhpreet Kaur is a PhD student at SITraN and member of the Neuroscience Institute. Traditionally, diagnosing dementia involves pen-and-paper tests that assess memory and thinking. However, these tests often miss subtle changes to memory, leading to delayed or missed diagnoses. is an automated tool that uses a human-like future to ask patients about their health, similar to traditional tests. The responses are analysed using artificial intelligence and machine learning to find early signs of memory problems and those at risk of developing dementia. This tool is over 90 per cent accurate, easy to use, cost-effective, and can be used remotely from home.

How does social isolation impact cognition in people with dementia?

James Myers is a PhD student in the school of Psychology and member of the Neuroscience Institute. Social isolation is a known risk factor for dementia, while social isolation and loneliness are associated with cognitive decline in older adults, but less is known about their impact on dementia patients throughout their diagnosis. James presented the findings of two studies based on electronic health records to observe how patients’ cognition changed over time and how this change was associated with social isolation or loneliness. Findings from both studies suggest that social isolation and loneliness can impact cognition throughout diagnosis duration and should be considered when looking at patient care.

The Tasty Spoon: Enhancing meal experiences for people with dementia

Dr Christian Morgner is a Senior Lecturer in Cultural and Creative Industries and the ºù«Ӱҵ University Management School and member of the Healthy Lifespan Institute. The most common public perception of dementia is to associate it primarily with memory loss but research suggests that the decline in taste occurs much earlier than memory loss. Dr Morgner discussed the impact of the loss of taste on people with dementia, such as high levels of malnutrition or the tendency to use salt and taste to compensate for lack of flavour. He presented results from a research and commercialisation project called the Tasty Spoon. The innovative spoon uses electrostimulation to help people with dementia differentiate between various types of food, restoring an enriched meal experience without the need for added salt or sugar.

Open network for frontotemporal dementia inflammation research; ON-FIRE study

Dr Simon Bell is a NIHR Clinical Lecturer in Neurology and a member of the Neuroscience Institute. There is long-running inflammation in brains with Frontotemporal dementia - suggesting that anti-inflammatory treatments might slow or prevent decline. However, no two people are the same in their symptoms or in what drives inflammation. Dr Bell presented a project that will involve a national study aiming to involve people with Frontotemporal dementia and including communities and remote areas that are too often under-represented in research. This project is the best way to measure inflammation in people with Frontotemporal dementia, and its causes. The open network will also build collaborations and trusted relationships to facilitate clinical trials of new drugs.