Neuroprotective peptides are promising candidate molecules for the treatment of Alzheimer's disease (AD). Oral application of KED (Lys-Glu-Asp) improved memory and attention in elderly individuals with functional CNS disorders. Peptide KED also restores synaptic plasticity in in vitro model of AD. This review is focused on the analysis of the influence of KED peptide on the expression of genes and synthesis of proteins regulating apoptosis, aging, neurogenesis, and involved in AD pathogenesis. Analysis of published reports and our experimental findings suggests that KED regulates the expression of genes of cell aging and apoptosis (р16, р21), genes (NES, GAP43) and proteins (nestin, GAP43) of the neuronal differentiation, and genes involved in AD pathogenesis (SUMO, APOE, and IGF1). The study the effectiveness of neuroprotective peptide KED in animal models of AD seems to be very important.

中文翻译：

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肽 KED：阿尔茨海默病神经发生调节的分子遗传学方面。

神经保护肽是治疗阿尔茨海默病 (AD) 的有希望的候选分子。口服 KED (Lys-Glu-Asp) 可改善患有功能性中枢神经系统疾病的老年人的记忆力和注意力。肽 KED 还恢复 AD 体外模型中的突触可塑性。本综述重点分析KED肽对调节细胞凋亡、衰老、神经发生和参与AD发病机制的基因表达和蛋白质合成的影响。对已发表的报告和我们的实验结果的分析表明，KED 调节细胞衰老和凋亡基因（第 16 条，第 21 条）、神经元分化的基因（NES、GAP43）和蛋白质（巢蛋白、GAP43）以及参与 AD 的基因的表达发病机制（SUMO、APOE 和 IGF1）。