The term ‘vascular dementia’ (VaD) corresponds to a clinicoradiological syndrome that can be defined with more or less restriction. VaD can result from: (1) cortical or subcortical ischemic lesions related to the occlusion of large vessels, (2) lacunar infarcts with or without white-matter lesions at the subcortical level related to small-vessel diseases, (3) ischemic lesions related to hypoperfusion or anoxic-ischemic encephalopathy or (4) hemorrhagic lesions. The prevention of VaD is based on stroke prevention which implies risk factor manipulation and use of antithrombotic drugs among which the most widely used are antiplatelet drugs. The efficiency of these drugs to prevent cognitive impairment and dementia is not proven. Prospective studies are needed to investigate their potential in patients at risk of VaD: after ischemic stroke, in the presence of cognitive impairment of vascular origin or when MRI shows ‘silent’ ischemic white-matter lesions and/or infarcts.