In our ageing population, the number of people affected by neurodegenerative conditions is increasing and, in a chain reaction, carers, the community and the economy are also suffering. At Manchester, we recognise the importance of reducing the burden neurodegenerative conditions place on society.
We were the first to phenotype fronto-temporal dementia; we were one of the first groups to conduct an amyloid PET scan in Alzheimer’s disease patients, and we were one of the first groups to identify inflammation as a key mediator of neuronal injury in stroke.
We have expertise across the board in neurodegenerative conditions, from genetics through to cognitive neuroscience and clinical application, while our close links with patients and clinicians in Manchester help us to use real-world practices to drive our research. The world works better with us.
From clinical and pathological characterisation, to identifying genes that cause the disease, The University of Manchester has sat at the forefront of research in FTD for the past 25 years.
We were the first to phenotype FTD and helped to identify the first gene for FTD, the gene encoding the microtubule-associated protein tau (MAPT) linked to chromosome 17. We also played a key role in the international collaboration that identified a second gene mutation causing FTD linked to chromosome 17, the granulin gene.
These findings opened up new fields of biological research and helped to improve FTD diagnosis and treatment development.
Since these initial discoveries, we have contributed to the identification of other genes, including the recent discovery of a repeat expansion mutation in C9orf72; the most common genetic cause of FTD identified to date.
This finding also allowed us to demonstrate that FTD and motor neuron disease are part of the same disease spectrum.
Finding the genes involved in FTD opens the door to identifying the various pathways involved in the disease, improved diagnosis and potential therapeutic targets for the future. The direct impact of this disease focus and genetic expertise comes in the form of genetic tests for patients - and, for us, advanced knowledge of the underlying mechanisms that lead to dementia.
Through specialist expertise, we see the potential for broad impact. The world works better with us.
We’re making breakthroughs in the search for prognostic markers and treatments for the most common form of dementia.
Using state-of-the-art PET imaging capabilities here at Manchester, we have measured glucose metabolism in the brains of patients with mild cognitive impairment, discovering greater glucose metabolism impairment in patients who then go on to develop Alzheimer’s disease.
These measurements of brain activity could be a prognostic marker, used in the future to help detect Alzheimer’s disease in its earliest stages, or lead to improved clinical trials of new treatments to delay or prevent the disease.
After five years of investigations in collaboration with other universities, we have also helped to unlock the crystal structure of the enzyme kynurenine 3-monooxygense (KMO), inhibition of which leads to improvements in Huntington’s disease and Alzheimer’s disease phenotypes.
This discovery could lead to new drug therapies targeting neurodegenerative diseases such as Huntington's, Alzheimer's and Parkinson's disease.
We see the bigger picture. The world works better with us.
We don’t just focus on the neuroscience. We focus on what it means to the patient.
That's why we are not only exploring the underlying mechanisms of dementia, but also looking at the cognitive decline caused by dementia and the social impact this has. In the early stages of dementia, we are exploring the relationship between neuropsychological deficit and problems with everyday activity, to find ways in which carers can be guided to help patients maintain a degree of independence for a longer period of time. This could not only help people with dementia to live better, but could also have a positive impact on the cost for the state of managing dementia care.
Such interventions could reduce depression, which is common in these early disease stages, and slow down entry into nursing care. But most importantly, they could help to maintain the quality of life that patients often lose rapidly.
We are also extending the impact of our research and helping to shape policy through an initiative that looks at dementia-friendly neighbourhoods.
“The need for more research, improved diagnosis and better support is as great as ever.”
Alistair Burns, Vice Dean at The University of Manchester and National Clinical Director for Dementia at NHS England
We unite basic neuroscience with social care. The world works better with us.
Twenty years of dedicated stroke research allows us to focus firmly on the future of stroke interventions.
At Manchester we have a strong and proven track record in neuroinflammation, a key factor in the pathophysiology of stroke, and expertise in stroke across the whole translational pathway, from molecule to man.
We were one of the first groups to identify inflammation as a key mediator of neuronal injury in stroke and have been a leading group in exploring this over the last 20 years. Using a combination of basic science and state-of-the-art imaging techniques, we have developed clinically relevant models that give us insights into the complex mechanisms of stroke.
Using this research, we are aiming to identify early changes and biomarkers in stroke that could be targets for future pharmaceutical intervention. These findings could lead to potential treatments for the effects of stoke, limiting its impact and helping patients to make a full recovery.
We have already demonstrated direct translation from our preclinical work to man: a drug that has shown beneficial effects in our stroke models is now currently in clinical trials in both ischaemic stroke and subarachnoid haemorrhage.
Our understanding of the complex mechanisms of stroke is advancing drug discovery and clinical trials. The world works better with us.