Therapeutic effect of organoselenium dietary supplementation in a sporadic dementia of Alzheimer's type model in rats

Pinton, Simone; Brüning, César Augusto; Oliveira, Carla Elena Sartori; Prigol, Marina; Nogueira, Cristina W.

doi:10.1016/j.jnutbio.2012.06.012

Cited by 51 publications

(21 citation statements)

References 48 publications

(75 reference statements)

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“…We performed the step-down passive avoidance test to evaluate the efficacy of rosuvastatin in ameliorating cognitive impairment induced by high salt and cholesterol diet. The step-down latency was significantly less in the TC group as compared to the NC group which clearly indicates impairment of learning and memory in the TC group and is consistent with previous findings [57]. The latency increased linearly with increase in RSV dose which indicates that RSV ameliorated HSCD-induced cognitive impairment in a dose-dependent manner.…”

Section: Discussionsupporting

confidence: 90%

Rosuvastatin alleviates high-salt and cholesterol diet-induced cognitive impairment in rats via Nrf2–ARE pathway

et al. 2018

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Objective: The objectives of our study were to investigate the possible effect of rosuvastatin in ameliorating high salt and cholesterol diet (HSCD)-induced cognitive impairment and to also investigate its possible action via the Nrf2-ARE pathway. Methods: In silico studies were performed to check the theoretical binding of rosuvastatin to the Nrf2 target. HSCD was used to induce cognitive impairment in rats and neurobehavioral studies were performed to evaluate the efficacy of rosuvastatin in enhancing cognition. Biochemical analyses were used to estimate changes in oxidative markers. Western blot and immunohistochemical analyses were done to check Nrf2 translocation. TUNEL and caspase 3 tests were performed to evaluate reversal of apoptosis by rosuvastatin. Results: Rosuvastatin showed good theoretical affinity to Nrf2, significantly reversed changes in oxidative biomarkers which were induced by HSCD, and also improved the performance of rats in the neurobehavioral test. A rise in nuclear translocation of Nrf2 was revealed through immunohistochemical analysis and western blot. TUNEL staining and caspase 3 activity showed attenuation of apoptosis. Discussion: We have investigated a novel mechanism of action for rosuvastatin (via the Nrf2-ARE pathway) and demonstrated that it has the potential to be used in the treatment of cognitive impairment. KEYWORDSCognitive impairment; rosuvastatin; high-salt and cholesterol diet; oxidative stress; Nrf2; nuclear factor (erythroid-derived 2)-like 2

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Section: Discussionsupporting

confidence: 90%

Rosuvastatin alleviates high-salt and cholesterol diet-induced cognitive impairment in rats via Nrf2–ARE pathway

et al. 2018

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“…139 Organoselenium compounds also display interesting effects in improving AD pathology in murine models: p, p 0 -methoxyl-diphenyl diselenide treatment to streptozotocinexposed mice slowed memory decline, reduced oxidative stress and normalised acetyl-cholinesterase activity. 140 Seleniumcontaining 8-hydroxyquinoline derivates bound to Cu 2+ , Fe 2+ and Zn 2+ inhibited aggregation and disassembled Cu 2+ -induced aggregates of Ab. 141 Some studies have shown an association between certain selenoproteins and pathological features of AD.…”

Section: Alzheimer's Diseasementioning

confidence: 99%

Selenium, selenoproteins and neurodegenerative diseases

et al. 2015

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It is unsurprising that our understanding of the role of selenium in neurological function is somewhat immature, considering its relatively recent discovery as an essential element to human health. Selenocysteine, the 21st amino acid, is the defining feature of the 25 selenoprotein-encoding genes so far discovered within the human genome. The low abundance of these proteins in the brain belies the integral role they play in normal neurological function, from well-characterised antioxidant activity in the periphery to poorly understood mechanisms that modulate mitochondrial function and response to brain pathology. Selenium has been identified as playing a role in several neurodegenerative disorders, including Alzheimer's and Parkinson's disease, though its function as a 'cause or effect' of disease process remains unclear. This review discusses selenium metabolism in detail, specifically with regard to the role it plays within the central nervous system, and examines the most current literature investigating how selenium may be involved in chronic diseases of the central nervous system.

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“…The glutathione peroxidase mimetic and organoselenium compound ebselen can reduce tau phosphorylation [42]. Other synthetic organoselenium compounds can improve cognitive impairments induced by streptozotocin and amyloid-β [43–46], and inhibit Cu-induced amyloid-β aggregates [47]. In contrast to supplementation studies, selenium deficiency increases amyloid-β deposition in an Alzheimer’s disease mouse model [48].…”

Section: Discussionmentioning

confidence: 99%

Selenoprotein S Reduces Endoplasmic Reticulum Stress-Induced Phosphorylation of Tau: Potential Role in Selenate Mitigation of Tau Pathology

Rueli

Torres

Dewing

et al. 2016

JAD

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Previous studies demonstrated that selenium in the form of sodium selenate reduces neurofibrillary tangle formation in Alzheimer’s disease models. Hyperphosphorylation of tau, which leads to formation of neurofibrillary tangles in Alzheimer’s disease, is increased by endoplasmic reticulum (ER) stress. Selenoprotein S (SelS) is part of an ER membrane complex that removes misfolded proteins from the ER as a means to reduce ER stress. Selenate, as with other forms of selenium, will increase selenoprotein expression. We therefore proposed that increased SelS expression by selenate would contribute to the beneficial actions of selenate in Alzheimer’s disease. SelS expression increased with ER stress and decreased under conditions of elevated glucose concentrations in the SH-SY5Y neuronal cell line. Reducing expression of SelS with siRNA promoted cell death in response to ER stress. Selenate increased SelS expression, which significantly correlated with decreased tau phosphorylation. Restricting SelS expression during ER stress conditions increased tau phosphorylation, and also promoted aggregation of phosphorylated tau in neurites and soma. In human postmortem brain, SelS expression coincided with neurofibrillary tangles, but not with amyloid-β plaques. These results indicate that selenate can alter phosphorylation of tau by increasing expression of SelS in Alzheimer’s disease and potentially other neurodegenerative disorders.

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Therapeutic effect of organoselenium dietary supplementation in a sporadic dementia of Alzheimer's type model in rats

Cited by 51 publications

References 48 publications

Rosuvastatin alleviates high-salt and cholesterol diet-induced cognitive impairment in rats via Nrf2–ARE pathway

Rosuvastatin alleviates high-salt and cholesterol diet-induced cognitive impairment in rats via Nrf2–ARE pathway

Selenium, selenoproteins and neurodegenerative diseases

Selenoprotein S Reduces Endoplasmic Reticulum Stress-Induced Phosphorylation of Tau: Potential Role in Selenate Mitigation of Tau Pathology

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