An emerging body of evidence indicates that beta -hydroxy-beta -methylgluta
ryl coenzyme A (HMG-CoA) reductase inhibitors, or 'statins', provide neurop
rotection in addition to reducing ischaemic stroke. Statins reduce the inci
dence of ischaemic stroke by stabilising atherosclerotic plaques in the pre
cerebral vasculature and through antithrombotic actions, and the neuroprote
ctive effects of statins may confer significant clinical benefit. Some of t
hese neuroprotective effects are likely to be cholesterol independent and m
ediated by the interruption of isoprenoid biosynthesis. Therapy with statin
s may modulate endothelial function and preserve blood flow to regions expo
sed to an ischaemic insult. In particular, statin-mediated preservation of
endothelial nitric oxide synthase activity in cerebral vasculature, especia
lly in the ischaemic penumbra, may limit neurological deficit. Moreover, pu
tative anti-inflammatory and antioxidant properties of statins may confer a
dditional neuroprotection. Further large clinical trials are necessary to a
ddress the role of statin therapy in the primary prevention of stroke, smal
l vessel cerebrovascular disease and vascular dementia.