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RESEARCH

research philosophy

Our research philosophy is that rigorous clinical observation and investigation provides insights into the causes of disease and modifiers of outcome which can improve clinical practice and can also be 'back-translated' to inform lab-based studies of aetiology. Better clinical phenotyping of stroke and dementia improves management and facilitates understanding of aetiology and better prognostication leads to more effective targeting of preventive treatment. Better understanding of the few major risk factors that are known to account for the majority of stroke and vascular dementia will yield greater dividends than the elucidation of many other 'novel' but relatively unimportant risk factors

Research aim

Our research aim to reduce the clinical burden of stroke and dementia has four key elements:

  1. Delay clinical onset by a few years:  The number of older people disabled by stroke will treble by 2050 if incidence is not reduced. Neuronal loss in stroke or dementia cannot yet be reversed, but age-related vascular disease can be slowed and end organ damage thereby delayed.  A 5-year delay in onset of stroke and dementia in the UK by 2050 would reduce the person-years lived with related disability by 50%.
  2. Focus on vascular risk factors: We have no disease-modifying treatments for neurodegeneration, but midlife vascular risk factors are strongly associated with risk of dementia and end-organ damage due to vascular disease is highly amenable to prevention. 
  3. Address pragmatic clinical questions: Clinical onset can be delayed if earlier recognition of risk and more reliable prognostication leads to more effective use of preventive treatments. We aim to improve early recognition of risk using clinical data, brain/vascular imaging, blood biomarkers and remote monitoring of risk factors.
  4. Do reliably powered mechanistic studies: Brain imaging and neuropathology are crucial to understanding mechanisms of cerebrovascular diseases and neurodegeneration, but most studies are underpowered, leading to conflicting results. We use the large clinical cohorts, biobanks and brain banks that we have established over the last 20 years to do studies that are powered to answer questions reliably.

Research Tools

Our research tools include:

  1. Large population-based studies and ‘big data’ to better understand risk factors and to better target preventive treatment;
  2. Randomised trials to better understand the effects of treatments;
  3. New monitoring technologies to improve diagnosis, prognostication, treatment and trials;
  4. Brain and vascular imaging to better understand aetiology and prognosis;
  5. Blood biomarker and genetic studies to better understand aetiology.

 

 

IMPACT ON CLINICAL PRACTICE

Our research has led to major changes in clinical practice and clinical guidelines on multiple aspects of primary and secondary prevention of stroke, including:

  • Prevention of stroke in patients with recently symptomatic carotid stenosis
  • Urgency of assessment and investigation of patients with TIA and minor stroke
  • Effective secondary prevention after TIA and minor stroke
  • Diagnosis and treatment of hypertension in prevention of stroke

Current work on risk factors for vascular dementia and on the long-term effects of aspirin on non-vascular disease will also change practice, and work on use of risk models to better target treatments at individuals has had a major impact on thinking about the application of the results of research in routine clinical practice.