Small vessel diseases and vascular contributions to neurodegeneration and dementia

Award Number
Research grant
Status / Stage
1 September 2017 -
31 December 2100
Duration (calculated)
83 years 03 months
Funding Amount
Funder/Grant study page
Contracted Centre
UK Dementia Research Institute at University of Edinburgh
Contracted Centre Webpage
Principal Investigator
Professor Joanna Wardlaw
PI Contact
WHO Catergories
Understanding risk factors
Understanding Underlying Disease
Disease Type
Dementia (Unspecified)

CPEC Review Info
Reference ID247
ResearcherReside Team


Award NumberUKDRI-4002
Status / StageActive
Start Date20170901
End Date21001231
Duration (calculated) 83 years 03 months
Funder/Grant study pageMRC UKRI
Contracted CentreUK Dementia Research Institute at University of Edinburgh
Contracted Centre Webpage
Funding Amount£966,674.00


The UK Dementia Research Institute (UK DRI) is an initiative funded by the Medical Research Council, Alzheimer’s Society and Alzheimer’s Research UK. Funding details for UK DRI programmes will be added in 2019. Clinical impact: Small vessel diseases (SVD) affect perforating cerebral vessels less than 500 microns in diameter resulting in diverse brain disorders. They cause most vascular dementia and worsen Alzheimer’s disease (AD), in total causing up to 45% of dementias. SVD also causes 25% of ischaemic and 90% of haemorrhagic strokes,1 worsens stroke outcome,2 and increases future risk of dementia, stroke and death.3 Patients present to different services, resulting in lack of awareness of SVD’s wide impact on the brain, mechanistic understanding or effective interventions.4 SVD and neurodegeneration: Visible SVD lesions, e.g. white matter hyperintensities (WMH), lacunes, microbleeds, perivascular spaces (PVS), recent small subcortical (lacunar) infarcts, atrophy,5 share clinical effects, epidemiology, pathology, and occur in AD6 as does microvessel dysfunction.6,7,8 SVD affects the brain diffusely: peri-lesion white matter is abnormal;9 global white matter integrity declines as SVD burden increases;10 SVD lesions cause focal/regional cortical,11 long tract and global brain atrophy.1 SVD is dynamic: acute lesions can disappear, remain a WMH or cavitate;1 WMH increase12 and regress, both in sporadic13 and monogenic SVDs.14 Although lesion dynamics are poorly understood, progression worsens cognition and physical function, while regression resulted in less cognitive decline, disability or recurrent stroke in our cohort9 (in review).