RT Journal Article
SR Electronic
T1 Updates on vascular dementia
JF Stroke and Vascular Neurology
JO Stroke Vasc Neurol
FD BMJ Publishing Group Ltd
SP svn-2025-004048
DO 10.1136/svn-2025-004048
A1 Ng, Sabrina
A1 Hornblass, Ava
A1 Habibi, Parnian
A1 Ikramuddin, Salman
A1 Chen, Jeffrey
A1 Feng, Wayne
A1 Cai, Dongming
YR 2025
UL http://svn.bmj.com/content/early/2025/02/24/svn-2025-004048.abstract
AB Vascular dementia (VaD) is the second leading cause of dementia after Alzheimer’s disease (AD). In comparison to AD, there is a decline in the incidence of VaD due to recent improvements in cardiovascular risk factors. Brain hypoperfusion and hypoxia due to vascular pathologies have been postulated as the primary disease mechanism of VaD. However, other factors such as neuroinflammation may also contribute to the development of VaD. Non-modifiable and modifiable risk factors have been attributed to VaD. The clinical features overlapping between AD and VaD create significant challenges for physicians. Newly developed biomarkers may potentially help differentiate VaD from other forms of dementia. Unlike AD, there is no Food and Drug Administration-approved drug or device for treating VaD. Current treatment options mainly target symptoms rather than slowing the development or progression of VaD. There are ongoing research studies testing the efficacy of various therapeutic strategies for VaD. In this narrative review, we will summarise current findings on epidemiology, attributed risk factors and disease mechanisms, as well as emphasise the importance of optimising lifestyle modifications and comorbid condition management in preventing or slowing down the development of VaD. Finally, current therapies and ongoing research studies of novel therapeutic interventions such as stem-cell therapy and neuromodulation are highlighted.