[Molecular and clinical aspects of the effect of cytidyndiphosphocholine on cognitive functions]. / Molekulyarnye i klinicheskie aspekty deistviya tsitidindifosfokholina na kognitivnye funktsii.

OBJECTIVE: Systematization of the array of publications on cytidyldiphosphocholine (CDP-choline). MATERIAL AND METHODS: Systematic computer analysis of all currently available publications on CDP-choline (1750 publications in PUBMED) using the topological theory of big data analysis. RESULTS: CDP-choline is essential for acetylcholine biosynthesis, phospholipid metabolism, and DNA methylation. The article describes the effects of CDP-choline on acetylcholinergic and other types of neurotransmission, anti-inflammatory, neuroprotective and neurotrophic effects of CDP-choline. Also, the paper presents the effects of the molecule on lipid metabolism and gene expression within the post-genomic paradigm (in particular, an increase in the expression of nicotinic and muscarinic acetylcholine receptors). The results of fundamental and clinical studies of CDP-choline in the treatment of cognitive impairments associated with cerebral ischemia and neurodegeneration are presented. CONCLUSION: The pharmacological effects of CDP-choline are mediated through multiple molecular mechanisms that contribute to the nootropic action of this molecule.

[Neurotrophic peptides of сerebrolysin as a basis for anticonvulsant effect of the drug]. / Neirotroficheskie peptidy tserebrolizina kak osnova protivosudorozhnogo potentsiala preparata.

AIM: To study an effect of cerebrolysin on the expression and severity of primary-generalized seizures caused by thiosemicarbazide and to analyze the corresponding molecular mechanisms. MATERIAL AND METHODS: The effects of cerebrolysin were studied on the thiosemicarbazide model of convulsions in 144 male rats. Cerebrolysin was introduced intraperitoneally in the dose of 2.5 ml/kg of body mass 5 days a week during 18 days. RESULTS AND CONCLUSION: Cerebrolysin reduces the severity and duration of seizures caused by thiosemicarbazide and increases the survival rate of animals. Cerebrolysin potentiates the anticonvulsant action of gabapentin and sodium valproate. Neurohistological analysis has shown that the thiosemicarbazide model results in the ischemic brain damage. Cerebrolysin substantially minimizes the ischemic injury of neurocytes induced by thiosemicarbazide and contributes to the restoration of brain tissue morphology.