اثرات محافظتی تمرین تناوبی با شدت بالا و مکمل کوآنزیم Q10 بر اختلال یادگیری و حافظه و شکل پذیری سیناپسی در مدل موش بیماری آلزایمر ناشی از بتا آمیلوئید. (Persian)

Introduction: Alzheimer’s disease (AD) as the commonest cause of dementia, poses a great socioeconomic burden on the community. We investigated the comparative effects of pretreatment with coenzyme Q10 (CoQ10) and highintensity interval training (HIIT) alone and in combination for eight continuous weeks, on the cognitive deficit, hippocampal synaptic plasticity, and amyloid-beta (Aβ) plaque formation in an AD rat model induced by an ICV microinjection of Aβ1-40. Methods and Materials: Eighty male Wistar rats were randomly assigned to the sham, control, Q10 (50 mg/kg; P.O), HIIT (high intensity: 4 min running at 85‑ 90% VO2max, low intensity: 3 min running at 50‑ 60% VO2max), Q10+HIIT, AD, vehicle, AD+Q10, AD+HIIT, and AD+Q10+HIIT groups. Results: The results showed that Aβ injection reduced cognitive functions in the Morris water maze (MWM) test, recognition memory in the novel object recognition test (NORT), and passive avoidance learning and memory (PAL) in the shuttle box test, which was accompanied by a decrease in total thiol groups (TTG), catalase (CAT), and glutathione peroxidase (GPx) activities, an increase in malondialdehyde (MDA) levels, and neuronal loss in the hippocampus. Interestingly, pretreatment with CoQ10, HIIT, or both, could markedly improve the oxidative status and cognitive decline in the MWM and NOR and PAL tests, and hinder neuronal loss in the hippocampus of Aβ- induced AD rats. There was a decrease in both components of LTP (PS amplitude and EPSP slope) and an increase in Aβ plaque production in the Aβ-induced rats. Interestingly, pretreatment with CoQ10, HIIT, or both could markedly ameliorate hippocampal LTP impairment and hinder Aβ plaque accumulation in the hippocampus in Aβ-induced rats. Conclusion: It can be stated that pretreatment with CoQ10, HIIT, or both improved Aβ-related behavioral deficits, probably through the alleviation of hippocampal synaptic dysfunction and inhibition of Aβ plaque generation. [ABSTRACT FROM AUTHOR]

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