The Science of Vascular Contributions to Cognitive Impairment and Dementia (VCID): A Framework for Advancing Research Priorities in the Cerebrovascular Biology of Cognitive Decline

Cell Mol Neurobiol. 2016 Mar;36(2):281-8. doi: 10.1007/s10571-016-0334-7. Epub 2016 Apr 19.


The World Health Organization reports that 47.5 million people are affected by dementia worldwide. With aging populations and 7.7 million new cases each year, the burden of illness due to dementia approaches crisis proportions. Despite significant advances in our understanding of the biology of Alzheimer's disease (AD), the leading dementia diagnosis, the actual causes of dementia in affected individuals are unknown except for rare fully penetrant genetic forms. Evidence from epidemiology and pathology studies indicates that damage to the vascular system is associated with an increased risk of many types of dementia. Both Alzheimer's pathology and cerebrovascular disease increase with age. How AD affects small blood vessel function and how vascular dysfunction contributes to the molecular pathology of Alzheimer's are areas of intense research. The science of vascular contributions to cognitive impairment and dementia (VCID) integrates diverse aspects of biology and incorporates the roles of multiple cell types that support the function of neural tissue. Because of the proven ability to prevent and treat cardiovascular disease and hypertension with population benefits for heart and stroke outcomes, it is proposed that understanding and targeting the biological mechanisms of VCID can have a similarly positive impact on public health.

Keywords: Alzheimer’s disease; Cardiovascular; Cerebrovascular; Vascular cognitive impairment, VCI; Vascular contributions to cognitive impairment and dementia, VCID; Vascular dementia.

Publication types

  • Review

MeSH terms

  • Animals
  • Cognitive Dysfunction / pathology*
  • Cost of Illness
  • Dementia, Vascular / diagnosis
  • Dementia, Vascular / pathology*
  • Humans
  • Models, Biological
  • Research*