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Hippocampal oxidative stress has a vital role in the pathophysiology of Alzheimer's disease (AD)-associated behavioral deficits. Ecdysterone (Ecdy), a natural product and primary steroid hormone, exhibits anti-oxidative and neuroprotective effects. High-intensity interval training (HIIT) has emerged as an effective method for improving physiological brain functions. The present study was designed to investigate the comparative effects of separate and combined HIIT and Ecdy treatment on behavioral functions, hippocampal oxidative status, histological changes in an amyloid-beta (Aβ)-induced rat model of AD. Adult male rats were treated simultaneously with HIIT exercise and Ecdy (10 mg/kg/day; P.O.), starting ten days after Aβ-injection, and they continued for eight consecutive weeks. At the end of the treatment course, the behavioral functions of the rats were assessed by commonly-used behavioral paradigms. Subsequently, brain samples were collected for histological analysis and hippocampus samples were collected for biochemical analysis. Results illustrated that Aβ injection impaired learning and memory performances in both novel object recognition and Barnes maze tests, reduced exploratory/locomotor activities in open field test, enhanced anxiety-like behavior in elevated plus-maze (P 0.05). These behavioral deficits accompanied hippocampal oxidative stress (decreased total antioxidant capacity content and glutathione peroxidase enzyme activity, increased total oxidant status and malondialdehyde level) and neuronal loss in the cerebral cortex and hippocampus in HE staining (P 0.05). HIIT and Ecdy improved anxiety-like behavior, attenuated total oxidant status and malondialdehyde, and prevented the neuronal loss (P 0.05). However, their combination resulted in a more complete and powerful improvement in all the above-mentioned Aβ-related deficits (P 0.05). Overall, these data provide evidence that a combination of HIIT and Ecdy treatment improves Aβ-induced behavioral deficits, possibly through ameliorating hippocampal oxidative status and preventing neuronal loss.

Alzheimer's disease (AD) is the most progressive form of neurodegenerative disease resulting in cognitive and non-cognitive deficits. Aluminum is recognized as a risk factor for the etiology, pathogenesis, and progression of AD. The present study was designed to determine the effects of p-coumaric acid (p-CA), a phenolic compound, on spatial cognitive ability and non-cognitive functions and to identify the role of oxidative stress and inflammation in an AD rat model induced by aluminum chloride (AlClBoth AlClThe results of this study showed that AlClThe findings suggest that both anti-oxidative and anti-inflammatory properties of p-CA may be the underlying mechanisms behind its beneficial effect in preventing neuronal loss and improving cognitive and non-cognitive deficits associated with AD.

Oxidative stress and neuronal death are the primary reasons for the progression of amyloid-beta (Aβ) deposition and cognitive deficits in Alzheimer's disease (AD). Ecdysterone (ecdy), a common derivative of ecdysteroids, possesses free radical scavenging and cognitive-improving effects. High-intensity interval training (HIIT) can be a therapeutic strategy for improving cognitive decline and oxidative stress. The present study was aimed to evaluate the effect of HIIT exercise and ecdy consumption synergistically on the changes in learning and memory functions, activities of hippocampal antioxidant enzymes, and neuronal population after AD induced by Aβ in male rats.Following ten days of Aβ injection, HIIT exercise and ecdy treatment (10 mg/kg/day; P.O.) were initiated and continued for eight consecutive weeks in rats. At the end of the treatment period, the rat's learning and memory functions were assessed using Morris water maze and passive avoidance tests. The activity of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GRx), and changes in neuronal population were evaluated in rats' brains.The results indicated that Aβ injection disrupted spatial/passive avoidance learning and memory in both tests, accompanied by a decrease in the SOD and CAT (as endogenous antioxidants) in rats' hippocampus. Additionally, Aβ injection resulted in neuronal loss in the cerebral cortex and hippocampus. Although the consumption of ecdy separately improved spatial/passive avoidance learning and memory impairments, recovered hippocampal activity of SOD, CAT, GRx, and prevented the hippocampal neuronal loss, its combination along with HIIT resulted in a more powerful and effective amelioration in all the above-mentioned Aβ-neuropathological changes.Our results confirm that a combination of HIIT and ecdy treatment could be a promising potential therapeutic option against AD-associated cognitive decline, owing to their free radical scavenging and neuroprotective properties.

Aims: Oxidative stress and neuronal death are the primary reasons for the progression of amyloid-beta (Aβ) deposition and cognitive deficits in Alzheimer’s disease (AD). Ecdysterone (Ecdy), a common derivative of ecdysteroids, possesses free radical scavenging and cognitive-improving effects. High-intensity interval training (HIIT) may be a therapeutic strategy for improving cognitive decline and oxidative stress. The present study was aimed to evaluate the effect of HIIT alone and its combination with Ecdysterone on the changes in learning and memory functions, hippocampal antioxidant enzymes activities, and neuronal population after AD induced by Aβ in male rats.Materials and methods: Following ten days of Aβ-injection, HIIT exercise and Ecdysterone treatment (10 mg/kg/day; P.O.) were initiated and continued for eight consecutive weeks in rats. At the end of the treatment period, rat’s learning and memory functions were assessed using water-maze and passive-avoidance tests. Moreover, the activity of superoxide dismutase (SOD), catalase (CAT), Glutathione Peroxidase (GPx), Glutathione Reductase (GRx) and neuronal population were evaluated in rat’s brains.Results: The results indicated that Aβ injection disrupted spatial/passive avoidance learning and memory in both water-maze and passive-avoidance paradigms, accompanied by a decrease in the superoxide dismutase and catalase (as endogenous antioxidants) in rat hippocampus. Additionally, Aβ injection resulted in neuronal loss in the cerebral cortex and hippocampus. Although consumption of Ecdysterone separately improved spatial/passive avoidance learning and memory impairments, recovered hippocampal activity of SOD, CAT, GRx, GRx and prevented the hippocampal neuronal loss, its combination with HIIT resulted in a more powerful and effective amelioration in all the above-mentioned Aβ-neuropathological changes.Conclusion: The current work's data confirms that a combination of HIIT exercise and Ecdysterone treatment could be a promising potential therapeutic agent against AD-associated cognitive decline, owing to their free radical scavenging and neuroprotective properties.

Aims Memory impairment is determined to be the most well-known symptom of Alzheimer's disease (AD). Although cell therapy seems is an efficient therapeutic strategy to attenuate the AD-related memory impairment, transplanted cells have a short lifespan and do not survive long term in the recipient animals. Herein, we investigated whether the combination therapy of Selenium nanoparticles (SeNPs) and stem cells attenuates the neurotoxicity in an AD animal model. Material and methods The adipose-derived mesenchymal stem cells (AMSCs) were transplanted in the AD model. In addition to cell injections, the animals also received oral administration of SeNPs (0.4 mg/kg) for one month. Recognition memory, cell survival, and BDNF concentration were assessed using the novel object recognition task, immunofluorescence, and ELISA methods. Key findings Our results showed that the combined therapy was more effective in increasing the discrimination index than the administering SeNPs or AMSCs alone. Moreover, SeNPs and stem cells together had the greatest effects in reducing the deposition of Aβ and increasing the concentration of BDNF. Ultimately, the survival and proliferation of transplanted cells were more in the group that received stem cells besides SeNPs. Significance Taken together, it seems that the transplantation of MSCs combined with SeNPs could achieve better results in the neuroprotection in the AD model than a conventional treatment of SeNPs or stem cells alone.