Using the rat Alzheimer's disease (AD)-like model we have analyzed the hippocampal short-term potentiation, levels of monoamines, and morphological changes in the hippocampal and cortical neurons after the administration of proteoglycans of embryonic origin (PEG). Results showed that the levels of monoamines and especially norepinephrine in the target AD brain structures were found elevated, except serotonin, which was unaffected in the hippocampus, but decreased in the frontal cortex. These changes were accompanied by the substantial structural damage of cortical and hippocampal neurons. PEG was able to reverse most of these changes. In addition, PEG administration had regime-dependent effects on a short-term potentiation pattern of hippocampal neurons. The elevated levels of key elements of brain monoaminergic system in the model of AD support the hypothesis of the important role of monoamines in the excessive synaptic excitation resulting in cognitive dysfunction in AD brain. The neuroprotective effect of PEG, as manifested by the recovery of the monoaminergic system, suggests this bioactive substance as a perspective therapeutic agent for the treatment of AD.

使用大鼠阿尔茨海默病 (AD) 样模型，我们分析了海马短期增强、单胺水平以及在施用胚胎来源的蛋白聚糖 (PEG) 后海马和皮质神经元的形态变化。结果表明，发现 AD 目标脑结构中单胺类物质，尤其是去甲肾上腺素的水平升高，但血清素除外，海马体中的血清素未受影响，但额叶皮层中的血清素水平下降。这些变化伴随着皮质和海马神经元的实质性结构损伤。PEG 能够逆转大部分这些变化。此外，PEG 给药对海马神经元的短期增强模式具有制度依赖性影响。AD模型中脑单胺能系统关键元素水平升高支持单胺在过度突触兴奋导致AD脑认知功能障碍中起重要作用的假设。PEG 的神经保护作用，表现为单胺能系统的恢复，表明这种生物活性物质可作为治疗 AD 的潜在治疗剂。