Exercise enhances the effectiveness of vitamin D therapy in rats with Alzheimer’s disease: emphasis on oxidative stress and inflammation

Medhat, Engy; Rashed, Laila Ahmed; Abdelgwad, Marwa; Aboulhoda, Basma Emad; Khalifa, Mohamed Mansour; El-Din, Shimaa Saad

doi:10.1007/s11011-019-00504-2

Cited by 29 publications

(14 citation statements)

References 49 publications

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“…Littlejohns et al discovered that there was strong association between the risk of AD and baseline vitamin D concentrations through both vascular and neurodegenerative mechanisms over a mean of 5.6 years follow up, whereas the optimal vitamin D level for general health remains to be determined [68]. The neuroprotective benefit of vitamin D was likely attributed to its anti-oxidant/anti-inflammatory effects [69] and exercise could enhance the efficacy of vitamin D therapy [70]. El-Din et al demonstrated that Nrf2 and its downstream anti-oxidant effectors were decreased in AD rats, while the neuro-inflammation as evidenced by TNF-α and phosphorylated ERK1/2 that led to the hyperphosphorylation of tau protein were increased (Fig.…”

Section: Vitamin Metabolismmentioning

confidence: 99%

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Chen

Wang²,

Wang

et al. 2020

Biomark Res

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Aging and average life expectancy have been increasing at a rapid rate, while there is an exponential risk to suffer from brain-related frailties and neurodegenerative diseases as the population ages. Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide with a projected expectation to blossom into the major challenge in elders and the cases are forecasted to increase about 3-fold in the next 40 years. Considering the etiological factors of AD are too complex to be completely understood, there is almost no effective cure to date, suggesting deeper pathomechanism insights are urgently needed. Metabolites are able to reflect the dynamic processes that are in progress or have happened, and metabolomic may therefore provide a more cost-effective and productive route to disease intervention, especially in the arena for pathomechanism exploration and new biomarker identification. In this review, we primarily focused on how redox signaling was involved in AD-related pathologies and the association between redox signaling and altered metabolic pathways. Moreover, we also expatiated the main redox signaling-associated mechanisms and their cross-talk that may be amenable to mechanism-based therapies. Five natural products with promising efficacy on AD inhibition and the benefit of AD intervention on its complications were highlighted as well. Graphical Abstract

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Section: Vitamin Metabolismmentioning

confidence: 99%

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Chen

Wang²,

Wang

et al. 2020

Biomark Res

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“…Additionally, a study by Briones also found that in patients with AD, the serum levels of IL-1β and 25(OH)D 3 showed a strong correlation ( Briones and Darwish, 2012 ). Another study also explored the effect of VD supplementation on ameliorating cognitive function through the antiinflammatory mechanism in vivo ( Medhat et al, 2020 ). Since deficiency in VD can be treated, VD may have an important public health inference in the prevention of age-related neurodegenerative diseases such as MCI and AD.…”

Section: Introductionmentioning

confidence: 99%

Mediation Effects of IL-1β and IL-18 on the Association Between Vitamin D Levels and Mild Cognitive Impairment Among Chinese Older Adults: A Case–Control Study in Taiyuan, China

Cheng

Dong

Song

et al. 2022

Front. Aging Neurosci.

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ObjectiveMild cognitive impairment (MCI) is a common, chronic, and complex disease in the elderly, which is often influenced by a variety of factors that include nutrition and inflammation. This study was undertaken to evaluate the mediation effects of inflammation on the association between vitamin D levels and MCI.MethodsWe explored the associations of inflammation and cognitive impairment related to 25(OH)D3 deficiency among 360 older people from the communities in China. Demographic characteristics, lifestyle, and health status were investigated by questionnaire, cognitive function was detected by MoCA, and plasma 25(OH)D3, interleukin-1β (IL-1β), and interleukin-18 (IL-18) were measured by ELISA. Spearman’s correlation analysis and logistic regression analysis were used to analyze the relationship among 25(OH)D3, IL-1β, and IL-18 in the MCI group and the control group and further to analyze the relationship between 25(OH)D3 and inflammatory factors in the MCI group. Finally, mediation analysis was performed to evaluate whether inflammation mediated the effect of 25(OH)D3 deficiency on cognitive impairment.ResultsThere were lower plasma 25(OH)D3 concentration and higher IL-1β and IL-18 levels in the MCI group compared with the controls. The levels of 25(OH)D3 were positively correlated with the MoCA scores and scores of different domains; the levels of IL-1β and IL-18 were negatively correlated with them (p < 0.05). In multivariate logistic analysis, there were significant associations among 25(OH)D3, IL-1β, IL-18, and MCI after adjusted. Further analysis revealed the significant association between the subjects with VD deficiency and the highest quartile of IL-18 in MCI (OR = 4.066), not with IL-1β after adjusting the confounding variables in MCI group. Ultimately, mediation analysis suggested that IL-1β and IL-18 could explain 25.4 and 17.5% of effect of the risk of cognitive impairment related to 25(OH)D3 deficiency.ConclusionOur findings suggested that 25(OH)D3 deficiency could increase the risk of cognitive impairment by a mechanism partly involving inflammation. Therefore, vitamin D supplementation may improve or delay the decline in cognitive function caused by inflammation in the elderly.

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“…2D to vitamin D receptor (VDR) in the nuclear; which begins a genetic response after reacting with RXR and producing Vitamin D response element (VDRE) [51,52]. VDRE binds to nuclear receptor coactivators (COACs) or corepressors (COREs) that increase BDNF and NGF gene expression [53]. Also, studies in MS patients shows increased free radical production, including nitric oxide that might exacerbate in ammatory reactions and brain lesions consequently due to the disrupted nicotinamide adenine dinucleotide phosphate (NADP+) system in MS patients [54,55].…”

Section: Discussionmentioning

confidence: 99%

The Compensatory Increased BDNF and NGF in Patients With Multiple Sclerosis Following Home-based Aerobic Training and Vitamin D Supplementation During the COVID-19 Outbreak

Bahmani

Hoseini

Amiri

2021

Preprint

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Background: Lifestyle modifications (physical activity and diet) are among the most promising strategies in MS rehabilitation. This study aimed to investigate the effect of home-based aerobic training and vitamin D supplementation in patients with multiple sclerosis during the COVID-19 outbreak.Methods: In this randomized, single-blinded, placebo-controlled trial, 38 females with Multiple sclerosis with EDSS: 3-5 (aged 20–40 years with body mass index [BMI] of 25–30 kg/m2) were randomly assigned into four groups: aerobic training + Vitamin D supplementation (AT+Vit D; n=10); aerobic training (AT; n=9); Vitamin D supplementation (Vit D; n=9), and Control (Placebo) (n=10). The AT program consisted of 50-70% of HRMax, 25-40 min/day, three days/wk for eight weeks. Participants in the Vit D group consumed 50000 IU of Vitamin D supplement capsules per week for eight weeks. The data were analyzed through paired t-test and one-way analysis of variance, as well as Tukey's post hoc test at the signification level of P<0.05.Results: BDNF and NGF levels improved significantly from pre-test to post-test within all experimental groups. BDNF and NGF decreased significantly in AT+Vit D, AT, and Vit D compared to C. Also, the results show that the AT+Vit D had significantly lower BDNF and NGF compared to AT (P=0.023 and P=0.011) and Vit D (P=0.001 and P=0.002). Conclusions: These findings suggest that the combination of AT+Vit D improves BDNF and NGF status more effectively than AT or Vit D alone in female Multiple sclerosis patients.

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Exercise enhances the effectiveness of vitamin D therapy in rats with Alzheimer’s disease: emphasis on oxidative stress and inflammation

Cited by 29 publications

References 49 publications

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Mediation Effects of IL-1β and IL-18 on the Association Between Vitamin D Levels and Mild Cognitive Impairment Among Chinese Older Adults: A Case–Control Study in Taiyuan, China

The Compensatory Increased BDNF and NGF in Patients With Multiple Sclerosis Following Home-based Aerobic Training and Vitamin D Supplementation During the COVID-19 Outbreak

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