Vascular dementia and vascular cognitive impairment-current treatments and future prospects.
- 1Stroke Research Group, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Abstract
Vascular cognitive impairment (VCI) and vascular dementia (VaD) represent a substantial and growing global health burden, yet remain under-recognized and comparatively under-researched. Two broad categories are post-stroke cognitive impairment, and VCI secondary to chronic cerebrovascular disease of which the most common cause is cerebral small vessel disease (SVD). In addition, cerebrovascular pathology frequently coexists with Alzheimer's disease (AD), increasing the probability that AD pathology will manifest as clinical dementia. Current management focuses primarily on prevention through modification of cardiovascular risk factors and lifestyle interventions. Intensive blood-pressure control has shown the strongest evidence, reducing future all-cause dementia while slowing progression of white-matter abnormalities. Multidomain lifestyle interventions incorporating exercise, diet, cognitive training, and vascular risk monitoring may also preserve cognition, although results across trials remain variable. In established VCI and VaD, treatment options are limited; cholinesterase inhibitors and memantine lack convincing evidence of benefit, and no pharmacological therapy has definitively demonstrated symptomatic improvement or delayed disease progression. Advances in understanding SVD and VCI pathophysiology are, however, identifying promising therapeutic targets. Emerging evidence highlights endothelial dysfunction, impaired cerebral autoregulation, increased blood-brain barrier permeability, inflammation, and glymphatic dysfunction as possible mechanisms underlying SVD. Current trials are evaluating treatment approaches based on this framework including cerebral vasodilators such as cilostazol, isosorbide mononitrate and phosphodiesterase-5 inhibitors, anti-inflammatory therapies, glucagon-like peptide-1 receptor agonists, remote ischemic conditioning, and strategies targeting glymphatic function. Improved mechanistic understanding, appropriately targeted interventions, and adequately powered long-term clinical trials are required to translate these emerging approaches into effective treatments for VCI and VaD.
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BibTeX
@article{markus2026vascular,
title = {{Vascular dementia and vascular cognitive impairment-current treatments and future prospects.}},
author = {Hugh S Markus},
journal = {International journal of stroke : official journal of the International Stroke Society},
year = {2026},
month = oct,
doi = {10.1177/17474930261492876},
url = {https://europepmc.org/article/MED/42894468},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Vascular dementia and vascular cognitive impairment-current treatments and future prospects.
AU - Hugh S Markus
PY - 2026
DA - 2026/10/19
JO - International journal of stroke : official journal of the International Stroke Society
DO - 10.1177/17474930261492876
UR - https://europepmc.org/article/MED/42894468
AB - Vascular cognitive impairment (VCI) and vascular dementia (VaD) represent a substantial and growing global health burden, yet remain under-recognized and comparatively under-researched. Two broad categories are post-stroke cognitive impairment, and VCI secondary to chronic cerebrovascular disease of which the most common cause is cerebral small vessel disease (SVD). In addition, cerebrovascular pathology frequently coexists with Alzheimer's disease (AD), increasing the probability that AD pathology will manifest as clinical dementia. Current management focuses primarily on prevention through modification of cardiovascular risk factors and lifestyle interventions. Intensive blood-pressure control has shown the strongest evidence, reducing future all-cause dementia while slowing progression of white-matter abnormalities. Multidomain lifestyle interventions incorporating exercise, diet, cognitive training, and vascular risk monitoring may also preserve cognition, although results across trials remain variable. In established VCI and VaD, treatment options are limited; cholinesterase inhibitors and memantine lack convincing evidence of benefit, and no pharmacological therapy has definitively demonstrated symptomatic improvement or delayed disease progression. Advances in understanding SVD and VCI pathophysiology are, however, identifying promising therapeutic targets. Emerging evidence highlights endothelial dysfunction, impaired cerebral autoregulation, increased blood-brain barrier permeability, inflammation, and glymphatic dysfunction as possible mechanisms underlying SVD. Current trials are evaluating treatment approaches based on this framework including cerebral vasodilators such as cilostazol, isosorbide mononitrate and phosphodiesterase-5 inhibitors, anti-inflammatory therapies, glucagon-like peptide-1 receptor agonists, remote ischemic conditioning, and strategies targeting glymphatic function. Improved mechanistic understanding, appropriately targeted interventions, and adequately powered long-term clinical trials are required to translate these emerging approaches into effective treatments for VCI and VaD.
SN - 1747-4930
SN - 1747-4949
ER -