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It was found that in the development of cerebral insufficiency in children who underwent pre- and perinatal hypoxia are the processes of neurodestruction associated with the activation of transmitter autocoidosis, oxidative and nitrosative stress and impairment of energy metabolism against the background of dysfunction of the myochondria. Experiments and clinics have demonstrated a direct dependence of the concentration of a number of neurospecific proteins and antibodies to them, molecular markers of oxidative stress and mitochondrial dysfunction in the blood of newborns on the severity of the clinical condition. The only neuromolecules that have the ability to resist the mechanisms of neurodestruction are considered to be neurotrophic factors and heat shock proteins, as well as factors induced by hypoxia. Accumulated preclinical and clinical data indicate that dysfunction in the synthesis of nerve growth factor (NGF), brain neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) may promote brain development with impaired neuroplasticity leading to cerebral insufficiency in children who have had pre- and perinatal hypoxia. Preclinical studies also revealed the neuroprotective role of HSP70 and HIF-1a in conditions of cerebral ischemia and hypoxia. A direct relationship was established between the concentration of HSP70, the severity of neurological disorders and the level of specific markers of neurodestruction. It has been shown that low concentrations of HSP70 contribute to the progression of neurodestruction.
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