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目的用快速老化小鼠(SAMP8)模拟老年痴呆,观察其学习记忆能力,并探讨其学习记忆能力下降的可能机制。方法采用10月龄SAMP8,并用同龄抗快速老化小鼠(SAMR1)作为正常对照。用水迷路检测近记忆以及空间学习记忆能力。用生物化学方法检测大脑皮层线粒体膜电位和ATP酶活力,观察线粒体功能;检测皮层和海马胆碱乙酰基转移酶(ChAT)和乙酰胆碱酯酶(AChE)的活力,观察中枢胆碱能神经功能;检测血清超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量,观察其全身性氧化应激状况。结果与SAMR1相比,SAMP8出现明显的衰老体征,其近记忆和空间学习记忆能力明显减弱,具有衰老和痴呆特征;皮层线粒体膜电位和ATP酶活力显著降低,海马ChAT活力显著下降,AChE活力显著升高,血清SOD活力稍有增高。结论SAMP8可以很好地模拟老年痴呆,其机制包括大脑皮层线粒体功能降低、海马胆碱能神经功能下降以及氧化应激等。
Objective To simulate Alzheimer’s disease with fast-aging mice (SAMP8) and to observe its learning and memory abilities, and to explore possible mechanisms of its decline in learning and memory. Methods 10-month-old SAMP8 was used, and the same age anti-aging mouse (SAMR1) was used as a normal control. Water lost to detect near memory and spatial learning and memory ability. The mitochondrial membrane potential and ATPase activity of the cerebral cortex were detected by biochemical methods and the mitochondrial function was observed. The activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) in cortex and hippocampus were detected to observe the function of central cholinergic nerve. Serum superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured to observe the status of systemic oxidative stress. Results Compared with SAMR1, SAMP8 showed obvious signs of aging. The memory and spatial learning and memory abilities of SAMP8 were significantly weakened, with the features of aging and dementia. The mitochondrial membrane potential and ATPase activity were significantly decreased, the activity of ChAT in hippocampus was significantly decreased, and the activity of AChE was significant Increased serum SOD activity slightly increased. Conclusions SAMP8 can simulate Alzheimer’s disease well. Its mechanisms include mitochondrial function decline in the cerebral cortex, decreased cholinergic function in hippocampus and oxidative stress.