Disruption of the blood flow to the brain, either a slow decline in supply due to vascular aging, or following a stroke, is an important contributing factor in the development of dementia. The brain requires a great deal of energy to function, and thus the supply of nutrients and oxygen is even more critical than is the case for other organs. Reductions in that supply have consequences.
Cerebrovascular diseases include a variety of medical conditions that affect the blood vessels of the brain and the cerebral circulation. These include conditions that may cause acute interruption of cerebral circulation and subsequent acute neuronal damage, such as ischaemic or haemorrhagic stroke, and disorders that may cause chronic pathological changes in small vessels and neurological dysfunction, such as cerebral small vessel diseases. Patients with cerebrovascular diseases, both acute and chronic, usually have multidimensional functional impairments to the brain and an increased risk of cognitive impairment and dementia.
Despite cognitive impairment after cerebral small vessel disease being a common cause of impairment of brain function, its underlying pathogenesis and mechanism are poorly understood. Recent studies showed that early impairment of cognition may be induced by disruption of the glio-neuro-vascular unit. Small vessel pathologies due to vascular risk factors may induce breakdown in the integrity of the blood-brain barrier and cerebral blood flow deficits. Although not yet tested in prospective longitudinal studies, structural and functional alterations of cerebral small vessels may trigger the cascade of molecular signals (for example, activation of innate immunity, vascular oxidative stress, and inflammation), leading to disruption of the glio-neuro-vascular unit. Neurovascular dysfunction alters the homeostasis of the brain microenvironment and promotes accumulation of amyloid and tau protein in regions involved in cognition, leading to early vascular and neurodegenerative cognitive impairment.
As cerebrovascular diseases and dementia are so closely interlinked, amelioration of vascular risk and vascular damage offers a new dawn for preventing not only vascular dementia but also mixed and even Alzheimer's dementias, and it may even offer alternative routes to clear amyloid and tau protein aggregation. For example, a substudy of the SPRINT MIND (Systolic Blood Pressure Intervention Trial Memory and Cognition in Decreased Hypertension) trial showed that intensive blood pressure reduction decreased progression of white matter hyperintensities, mild cognitive impairment, and probable dementia. The results of these trials indicated that patients with cerebrovascular disease or vascular risk factors might be a potential target population to prevent dementia.