背景:衰老是阿尔茨海默病(AD)的主要危险因素,认知和记忆障碍在老年人中很常见。有趣的是,辅酶Q10(Q10)水平在衰老动物的大脑中下降。Q10是一种重要的抗氧化物质,在线粒体中具有重要作用。
目的:我们评估了Q10对老年β-淀粉样蛋白(Aβ)诱导的AD大鼠学习记忆和突触可塑性的可能影响。
方法:在本研究中,将40只Wistar大鼠(24-36月龄;360-450g)随机分为四组(n=10只大鼠/组)-I组:对照组,第二组:Aβ,第三组:Q10;50mg/kg,和IV组:Q10+Aβ。在Aβ注射前,每天通过管饲法口服Q10,持续4周。通过新物体识别(NOR)测量大鼠的认知功能和学习记忆能力,莫里斯水迷宫(MWM),和被动回避学习(PAL)测试。最后,丙二醛(MDA),总抗氧化能力(TAC),总巯基(TTG),测量总氧化剂状态(TOS)。
结果:Q10改善了NOR检验中Aβ相关的判别指数下降,MWM测试中的空间学习和记忆,PAL测试中的被动回避学习和记忆,老年大鼠海马PP-DG通路的长时程增强(LTP)损伤。此外,Aβ注射显著增加血清MDA和TOS水平。Q10,显着逆转了这些参数,并且还增加了AβQ10组的TAC和TTG水平。
结论:我们的实验结果表明,补充Q10可以抑制神经变性的进展,否则会损害我们实验动物的学习和记忆并降低突触可塑性。因此,给予AD患者类似的Q10补充治疗可能为他们提供更好的生活质量.
BACKGROUND: Aging is the major risk factor for Alzheimer\'s disease (AD), and cognitive and memory impairments are common among the elderly. Interestingly, coenzyme Q10 (Q10) levels decline in the brain of aging animals. Q10 is a substantial antioxidant substance, which has an important role in the mitochondria.
OBJECTIVE: We assessed the possible effects of Q10 on learning and memory and synaptic plasticity in aged β-amyloid (Aβ)-induced AD rats.
METHODS: In this
study, 40 Wistar rats (24-36 months old; 360-450 g) were randomly assigned to four groups (n = 10 rats/group)-group I: control, group II: Aβ, group III: Q10; 50 mg/kg, and group IV: Q10+Aβ. Q10 was administered orally by gavage daily for 4 weeks before the Aβ injection. The cognitive function and learning and memory of the rats were measured by the novel object recognition (NOR), Morris water maze (MWM), and passive avoidance learning (PAL) tests. Finally, malondialdehyde (MDA), total antioxidant capacity (TAC), total thiol group (TTG), and total oxidant status (TOS) were measured.
RESULTS: Q10 improved the Aβ-related decrease in the discrimination index in the NOR test, spatial learning and memory in the MWM test, passive avoidance learning and memory in the PAL test, and long-term potentiation (LTP) impairment in the hippocampal PP-DG pathway in aged rats. In addition, Aβ injection significantly increased serum MDA and TOS levels. Q10, however, significantly reversed these parameters and also increased TAC and TTG levels in the Aβ+Q10 group.
CONCLUSIONS: Our experimental findings suggest that Q10 supplementation can suppress the progression of neurodegeneration that otherwise impairs learning and memory and reduces synaptic plasticity in our experimental animals. Therefore, similar supplemental Q10 treatment given to humans with AD could possibly provide them a better quality of life.