Whether Coenzyme Q10 modulates cognitive function, synaptic plasticity, learning, and memory impairment in elderly rats that received intracerebroventricular Aβ (Special attention to aging)

Background and Aim : Alzheimer’s disease (AD) is the most common cause of dementia and a great socioeconomic burden in the aging society. Considering that the primary risk factor for AD is old age, the prevalence of AD is increasing because of an increase in aging populations globally. Although the exact pathophysiology is still unknown, Molecular mechanisms of AD are converging on the notion mitochondrial dysfunction, oxidative stress, neuroinflammation, and accumulation of amyloid β (Aβ). Cognitive and memory deficits are common in older adults, interestingly; the concentration of Coenzyme Q10 (CoQ10) is decreased in the brain of aging animals. Therefore, the aim of the present study was to investigate the possible effects of CoQ10 on cognitive function, synaptic plasticity, learning, and memory in aged rats.Methods : In this study, 40 aged male Wistar rats (360–450 g, 24–36 months old) were assigned to four groups (n=10 rats/group): control group(saline), Aβ group; intraventricular Aβ injection, Q10 group; Q10 via oral gavage and Q10+Aβ group. Q10 was administered via oral gavage, once a day, for 4 weeks before the Aβ injection. The cognitive function, and learning memory of rats were evaluated using novel object recognition (NOR), Morris water maze and passive avoidance tests. Also in this study, in vivo electrophysiological recordings were performed to quantify the excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the hippocampal dentate gyrus. Long-term potentiation (LTP) was created by a high-frequency stimulation of the perforant pathway. LTP, a widely researched model of synaptic plasticity, which occurs during learning and memory, in rat model of AD.Results : The discrimination index of the NOR test in the Aβ groups receiving CoQ10 (Q10+Aβ) was significantly higher than that in the control group. In addition, the step through latency was significantly longer and the time spent in the dark compartment was significantly shorter in the Aβ groups receiving CoQ10 (Q10+Aβ) than in the Aβ group. Also Following LTP induction, the EPSP slope and PS amplitude were significantly diminished in Aβ-injected rats, compared with Q10 and control rats. Q10 treatment of Aβ-injected rats significantly attenuated these decreases, suggesting that Q10 reduces the effects of Aβ on LTP.Conclusion : The present findings suggested that CoQ10 supplementation treatment can improve, cognitive function, learning and memory, and hippocampal synaptic plasticity deficits induced by Aβ in older subjects via its up-regulating mitochondrial function, antioxidant, and anti-inflammatory activity. Thus CoQ10 supplementation has the potential to inhibit the progression of neurodegeneration, leading to a better quality of life for humans suffering with AD.

کلیدواژه ها:

Alzheimer’s disease ، aging ، Coenzyme Q10 ، Long-term potentiation ، learning and memory