Even in early studies on the ...

Even in early studies on Alzheimer's disease, was found decrease glucose transport through the blood-brain barrier. Due to decreased cerebral glucose metabolism caused by biochemical changes in the process of glycolysis, citrate cycle and electron transport chain, energy-substrates (primarily ATP) are produced in insufficient quantities. In vascular dementia, which is mainly a consequence of lacunar infarction and intracerebral lesions of small vessels ("Hypertensive leukoencephalopathy"), you may experience similar metabolic changes, although different from Alzheimer's disease etiology and pathogenic mechanisms. The result of the reduced supply of oxygen is the accumulation of lactate in the tissues, which leads to acidosis and the subsequent decline in enzyme activity. These data suggest a pathogenetic approach to treatment of dementia, the use of pharmacological agents that enhance the exchange of aerobic glucose. Such drugs include, for example, Actovegin - deproteinized gemodializat, derived from calf blood [2]. Thanks to special technology of making the product contains only low-molecular components of physiological constants. The latest figures contained in the product fraction inositol-fosfooligosaharidov responsible for the active action Actovegin on energy metabolism. Clinical studies have confirmed the efficacy of Actovegin in the treatment of various diseases, especially dementia. Impact on the pathogenesis of the disease three main responsible for the development of a positive therapeutic effect Actovegin against dementia: · Effects on glucose transport. Fraction of inositol-oligosaccharides (IOS) gemodializata activates glucose transporters located in the cell membrane. Increased flow of glucose across the blood-brain barrier into the brain cells. · A positive impact on glucose utilization. Patients with Alzheimer's disease, among other things, reduced activity of the enzyme pyruvate dehydrogenase (PDH). As a consequence, significantly reduced the conversion of glucose via pyruvate to acetyl-coenzyme A (acetyl-CoA). In turn, the acetyl-CoA is the substrate, which is included in the citric acid cycle and at the same time is a powerful stimulator of aerobic metabolism and energy production. In addition, acetyl-CoA is required for the formation of acetylcholine. Fraction of IPV in Actovegin has the ability to stimulate the activity of PDH, through which increases the formation of acetyl-CoA, which then enters the citrate cycle and electron transport chain for aerobic metabolism of glucose. Thus produced a greater amount of ATP, and not disruptive to the formation of neurotransmitters (Fig. 1). Fig. 1 Actovegin activates located in the cell membrane glucose transporters and increases the activity of pyruvate dehydrogenase (PDH). Increased transport of glucose into the cell and the synthesis of ATP • Better utilization of oxygen in cerebral mitochondria.