It is well known that synaptic plasticity is associated with cognitive performance in Alzheimer's disease (AD). Testosterone (T) is known to exert protective effects on cognitive deficits in AD, but the underlying mechanisms of androgenic action on synaptic plasticity remain unclear. Thus, the aim of this study was to examine the protective mechanism attributed to T on synaptic plasticity in an AD senescence accelerated mouse prone 8 (SAMP8) model. The following parameters were measured: (1) number of intact pyramidal cells in hippocampal CA1 region (2) phosphorylated N-methyl-D-aspartate receptor-1 (p-NMDAR1) and (3) phosphorylated calmodulin-dependent protein kinase II (p-CaMKII). In addition, the content of whole brain malondialdehyde (MDA) as well as activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined. Treatment with T significantly elevated the number of intact pyramidal cells in hippocampal CA1 region and markedly increased hippocampal protein and mRNA expression levels of p-NMDAR1 and p-CaMK II. Further, T significantly decreased whole brain MDA levels accompanied by elevated activities of SOD and GSH-Px. Data suggest that the protective effects of T on synaptic plasticity in a mouse AD model may be associated with reduction of oxidant stress.

中文翻译：

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睾丸激素抑制氧化应激可改善衰老加速小鼠的突触可塑性。

众所周知，在阿尔茨海默氏病（AD）中，突触可塑性与认知能力有关。已知睾丸激素（T）可以对AD的认知缺陷发挥保护作用，但是雄激素对突触可塑性的潜在作用机制尚不清楚。因此，本研究的目的是在AD衰老加速小鼠俯卧8（SAMP8）模型中研究归因于T的突触可塑性的保护机制。测量以下参数：（1）海马CA1区完整的锥体细胞数量（2）磷酸化的N-甲基-D-天冬氨酸受体1（p-NMDAR1）和（3）磷酸化的钙调蛋白依赖性蛋白激酶II（p -CaMKII）。此外，测定全脑丙二醛（MDA）的含量以及超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性。用T处理可显着提高海马CA1区完整锥体细胞的数量，并显着增加p-NMDAR1和p-CaMK II的海马蛋白和mRNA表达水平。此外，T显着降低了全脑MDA水平，并伴有SOD和GSH-Px活性升高。数据表明，T对小鼠AD模型中突触可塑性的保护作用可能与降低氧化应激有关。T显着降低全脑MDA水平，并伴有SOD和GSH-Px活性升高。数据表明，T对小鼠AD模型中突触可塑性的保护作用可能与降低氧化应激有关。T显着降低全脑MDA水平，并伴有SOD和GSH-Px活性升高。数据表明，T对小鼠AD模型中突触可塑性的保护作用可能与降低氧化应激有关。