Vascular dementia (VD) is not considered to be a separate disease with its own inherent pathology, although it there were several attempts to recognize the VD a separate disease. It is a heterogeneous syndrome, including several different clinical and pathological manifestations: preferential frontal brain cortex disorders with impairment of motor functions, attention and behavior.
In the pathogenesis of vascular dementia an activation of glutamatergic NMDA-receptors plays
a special role. Normally NMDA-receptors activation is connected with plasticity of the central nervous system structures, and it is responsible for learning and memory. However in pathological states a prolonged excessive activation of these receptors leads to neuronal cell death. At a supraspinal level the NMDA-receptors are localized in hippocampus, cortex of cerebral hemispheres (especially in anterior area), thalamus, striatum, cerebellum and brain stem, at the spinal level - mainly in the posterior horns in the substantia gelatinosa and in small quantities - in gray matter of spinal cord. Excessive activation of glutamate receptors is accompanied by a massive inflow of calcium and sodium ions into neurons, which leads to membrane depolarization and activation of voltage-dependent calcium channels and is accompanied by a greater increase of calcium ions entry to the cells.