Vascular cognitive impairment (VCI) and vascular dementia are the most common forms of cognitive disorder associated with cerebrovascular disease and related to increased morbidity and mortality among the older population. Growing evidence suggests the contribution of blood-pressure variability, cardiac arrhythmia, hyperactivation of the renin–angiotensin–aldosterone system, endothelial dysfunction, vascular remodeling and stiffness, different angiopathies, neural tissue homeostasis, and systemic metabolic disorders to the pathophysiology of VCI. In this review, we focus on factors contributing to cerebrovascular disease, neurovascular unit alterations, and novel approaches to cognitive improvement in patients with cognitive decline. One of the important factors associated with the neuronal causes of VCI is the S100B protein, which can affect the expression of cytokines in the brain, support homeostasis, and regulate processes of differentiation, repair, and apoptosis of the nervous tissue. Since the pathological basis of VCI is complex and diverse, treatment affecting the mechanisms of cognitive disorders should be developed. The prospective role of a novel complex drug consisting of released–active antibodies to S100 and to endothelial NO synthase in VCI treatment is highlighted.

Neurotic disorders (NDs) are among the most common mental diseases leading to a decrease in the quality of life, lack of socialization, and increased mortality. The diagnosis and treatment of all types of NDs are challenging. In the light of the ongoing search for an effective and safe therapeutic strategy influencing certain aspects of ND pathogenesis, technologically processed highly diluted antibodies to S100 protein (TP Abs to S100) seem to be a promising treatment option for patients with NDs. TP Abs to S100 possess stress-protective, anxiolytic, antidepressant, antiamnestic, and neuroprotective activities. In the current review, we describe the mechanisms of action and pharmacological effects of TP Abs to S100 demonstrated in nonclinical (preclinical) and clinical studies. Based on the data, we tried to evaluate the future prospects of the TP Abs to S100 as the drug of choice for ND treatment.

The use of divazа resulted in clinical improvement and normalization of markers of endothelial dysfunction as well.

The authors review the studies on oxidative stress in the pathogenesis of cerebrovascular diseases (CVD) and highlight a contribution of endothelial dysfunction to the CVD development. Own experience of using divasa in patients of old and very old age with chronic CVD comorbid to cerebral atherosclerosis is described.

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