Physiologically, the cerebral autoregulation system allows maintenance of constant cerebral blood fl ow over a wide range of blood pressure. In old people, there is a progressive reshape of cerebral autoregulation from a sigmoid curve to a straight line. This implies that any abrupt change in blood pressure will result in a rapid and signifi cant change in cerebral blood fl ow. Hypertension has often been observed to be a risk factor for vascular dementia (VaD) and sometimes for Alzheimer disease although not always. Indeed, high blood pressure may accelerate cerebral white matter lesions, but white matter lesions have been found to be facilitated by excessive fall in blood pressure, including orthostatic dysregulation and postprandial hypotension. Many recent studies observed among other data, that there was a correlation between systolic pressure reduction and cognitive decline in women, which was not accounted for by other factors. Baseline blood pressure level was not signifi cantly related to cognitive decline with initial good cognition. Some researchers speculate that blood pressure reduction might be an early change of the dementing process. The most confounding factor is that low pressure by itself might be a predictor of death; nevertheless, the effect of low blood pressure on cognition is underestimated because of a survival bias. Another explanation is that clinically unrecognized vascular lesions in the brain or atherosclerosis are responsible for both cognitive decline and blood pressure reduction. We discuss the entire process, and try to defi ne a possible mechanism that is able to explain the dynamic by which hypotension might be related to dementia. Keywords: vascular dementia, hypotension, low blood pressure, alzheimer disease As longevity increases worldwide, age-related dementias are burgeoning. Age-related cerebral degenerative changes are coupled therefore with decreased perfusion, usually assumed to be secondary to decreased cerebral metabolic demands (Meyer et al 1999). During aging, the declines in cerebral tissue densities of the gray cortex (polio-araiosis) and of the white matter (leuko-araiosis) refl ect neuronal degenerative changes, which progress concurrently with cerebral perfusion declines.In particular, leuko-araiosis correlates with advancing age, cerebral atrophy, hypoperfusion of white matter, and cognitive impairments (Meyer et al 2000). Leuko-araiosis is detectable in 9%-19% of older 'normal' subjects, but is virtually always present in vascular dementia (VaD). Of special interest are the data emerging from the study of Meyer and colleagues (2000): normative subjects destined for later cognitive decline had excessive leuko-araiosis at study entry, suggesting leuko-araiosis is, by itself, a risk factor for cognitive decline.Thus, the researchers are trying to defi ne the passage between normality, the so-called leuko-araiosis age-related and the excess of the response to the vascular damage, confi guring the dementia, as a clinical syndrome. White matter injury m...