Correction: D-galactose-induced brain ageing model: A systematic review and meta-analysis on cognitive outcomes and oxidative stress indices

Sadigh‐Eteghad, Saeed; Majdi, Alireza; McCann, Sarah; Mahmoudi, Javad; Vafaee, Manouchehr Seyedi; Macleod, Malcolm

doi:10.1371/journal.pone.0190328

Cited by 19 publications

(13 citation statements)

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“…Since the hippocampus plays a key role in the consolidation of memories related to spatial navigation, we subjected mice to the Barnes and Lashley III mazes as hippocampus-dependent spatial learning and memory tasks. The data showed that administration of D -galactose and global ischemia induction together significantly impaired spatial learning and memory, which is in line with previous reports ( Xu et al, 2000 ; Sadigh-Eteghad et al, 2017 ; Salehpour et al, 2017 ). On the other hand, 2 weeks of PBM and/or CoQ 10 treatments significantly reversed this deficiency.…”

Section: Discussionsupporting

confidence: 92%

“…As an alternative approach, we modeled natural aging by chronic administration of D -galactose to rodents. D -galactose is a reducing hexose sugar that enters the brain and reacts with many cellular components at high concentration, producing oxidative damage to lipids and DNA ( Ho et al, 2003 ; Sadigh-Eteghad et al, 2017 ). The chronic D -galactose treatment induces changes that resemble natural aging and mimics several characteristics of brain aging ( Wei et al, 2005 ; Sadigh-Eteghad et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

“…D -galactose is a reducing hexose sugar that enters the brain and reacts with many cellular components at high concentration, producing oxidative damage to lipids and DNA ( Ho et al, 2003 ; Sadigh-Eteghad et al, 2017 ). The chronic D -galactose treatment induces changes that resemble natural aging and mimics several characteristics of brain aging ( Wei et al, 2005 ; Sadigh-Eteghad et al, 2017 ). The administration to rodents has been shown to cause neurocognitive impairments, including memory deficits, increased inflammatory responses and mitochondrial dysfunction ( Shan et al, 2009 ; Sadigh-Eteghad et al, 2017 ; Salehpour et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

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Photobiomodulation and Coenzyme Q10 Treatments Attenuate Cognitive Impairment Associated With Model of Transient Global Brain Ischemia in Artificially Aged Mice

Salehpour

Farajdokht

Mahmoudi

et al. 2019

Front. Cell. Neurosci.

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Disturbances in mitochondrial biogenesis and bioenergetics, combined with neuroinflammation, play cardinal roles in the cognitive impairment during aging that is further exacerbated by transient cerebral ischemia. Both near-infrared (NIR) photobiomodulation (PBM) and Coenzyme Q10 (CoQ10) administration are known to stimulate mitochondrial electron transport that potentially may reverse the effects of cerebral ischemia in aged animals. We tested the hypothesis that the effects of PBM and CoQ10, separately or in combination, improve cognition in a mouse model of transient cerebral ischemia superimposed on a model of aging. We modeled aging by 6-week administration of D-galactose (500 mg/kg subcutaneous) to mice. We subsequently induced transient cerebral ischemia by bilateral occlusion of the common carotid artery (BCCAO). We treated the mice with PBM (810 nm transcranial laser) or CoQ10 (500 mg/kg by gavage), or both, for 2 weeks after surgery. We assessed cognitive function by the Barnes and Lashley III mazes and the What-Where-Which (WWWhich) task. PBM or CoQ10, and both, improved spatial and episodic memory in the mice. Separately and together, the treatments lowered reactive oxygen species and raised ATP and general mitochondrial activity as well as biomarkers of mitochondrial biogenesis, including SIRT1, PGC-1α, NRF1, and TFAM. Neuroinflammatory responsiveness declined, as indicated by decreased iNOS, TNF-α, and IL-1β levels with the PBM and CoQ10 treatments. Collectively, the findings of this preclinical study imply that the procognitive effects of NIR PBM and CoQ10 treatments, separately or in combination, are beneficial in a model of transient global brain ischemia superimposed on a model of aging in mice.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Photobiomodulation and Coenzyme Q10 Treatments Attenuate Cognitive Impairment Associated With Model of Transient Global Brain Ischemia in Artificially Aged Mice

Salehpour

Farajdokht

Mahmoudi

et al. 2019

Front. Cell. Neurosci.

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“…D-gal administration to mice is an established experimental model of aging-linked cognitive and behavior disorders and can be employed to study anti-aging drugs [ 5 ]. D-gal treated animals exhibited enhanced brain oxidative stress demonstrated to be involved in cognitive and behaviors abnormalities [ 5 , 21 ]. The current study demonstrated that CaD attenuated cognitive and behavioral impairments induced by D-gal through the control of lipid peroxidation and oxidative stress in brain tissue.…”

Section: Discussionmentioning

confidence: 99%

Calcium Dobesilate Reverses Cognitive Deficits and Anxiety-Like Behaviors in the D-Galactose-Induced Aging Mouse Model through Modulation of Oxidative Stress

et al. 2021

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The long-term treatment of mice with D-galactose (D-gal) induces the overproduction of reactive oxygen species (ROS) and is a well-accepted experimental model of oxidative stress-linked cognitive disorders in physiological aging. Calcium dobesilate (CaD, Doxium®) is an established vasoactive and angioprotective drug commonly used for the clinical treatment of diabetic retinopathy and chronic venous insufficiency. It has antioxidant properties and controls vascular permeability. In the current study, we evaluated the protective effects of CaD (50 and 100 mg/kg/day p.o.) in male mice treated with D-gal (500 mg/kg/day p.o.) for six weeks. Results demonstrated that body weight loss, anxiety-like and cognitive impairments of D-gal-treated animals were reversed by CaD administration as evaluated by the measurement of mice performance in elevated plus-maze, Y-maze, and shuttle box tests. CaD treatment also inhibited the oxidative stress in aging mouse brains by decreasing malondialdehyde (MDA) levels and increasing superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) enzyme activities. These results could open new perspectives for the clinical use of CaD in treating and preventing cognitive impairment in older people.

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“…Excessive D-galactose can cause increased metabolic rates in the body and more oxidative accumulation of free radicals, thus leading to damage to DNA, proteins, cell membrane lipids, and other macromolecules in cells, resulting in mitochondrial damage, nerve damage, and increased cognitive decline, thereby making the body age (28). D-galactose-induced premature aging animal models are similar to natural aging in terms of physiological and biochemical indicators, so they are widely used in drug screens and evaluations of anti-aging food products (29).…”

Section: Discussionmentioning

confidence: 99%

Antioxidant Effect of Soymilk Fermented by Lactobacillus plantarum HFY01 on D-Galactose-Induced Premature Aging Mouse Model

Fan

et al. 2021

Front. Nutr.

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The antioxidant effect of soymilk fermented by Lactobacillus plantarum HFY01 (screened from yak yogurt) was investigated on mice with premature aging induced by D-galactose. In vitro antioxidant results showed that L. plantarum HFY01-fermented soymilk (LP-HFY01-DR) had better ability to scavenge the free radicals 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2′-azino-bis (3-ethylbenzthiazoline-6-sulphonic acid) diammonium salt (ABTS) than unfermented soymilk and Lactobacillus bulgaricus-fermented soymilk. Histopathological observation showed that LP-HFY01-DR could protect the skin, spleen and liver, reduce oxidative damage and inflammation. Biochemical results showed that LP-HFY01-DR could effectively upregulate glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels and decrease malondialdehyde (MDA) content in the liver, brain, and serum. Real-time quantitative reverse transcription polymerase chain reaction further showed that LP-HFY01-DR could promote the relative expression levels of the genes encoding for cuprozinc superoxide dismutase (Cu/Zn-SOD, SOD1), manganese superoxide dismutase (Mn-SOD, SOD2), CAT, GSH, and GSH-Px in the liver, spleen, and skin. High-performance liquid chromatography results revealed daidzin, glycitin, genistin, daidzein, glycitein, and genistein in LP-HFY01-DR. In conclusion, LP-HFY01-DR could improve the antioxidant capacity in mice with premature aging induced by D-galactose.

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Correction: D-galactose-induced brain ageing model: A systematic review and meta-analysis on cognitive outcomes and oxidative stress indices

Cited by 19 publications

References 1 publication

Photobiomodulation and Coenzyme Q10 Treatments Attenuate Cognitive Impairment Associated With Model of Transient Global Brain Ischemia in Artificially Aged Mice

Photobiomodulation and Coenzyme Q10 Treatments Attenuate Cognitive Impairment Associated With Model of Transient Global Brain Ischemia in Artificially Aged Mice

Calcium Dobesilate Reverses Cognitive Deficits and Anxiety-Like Behaviors in the D-Galactose-Induced Aging Mouse Model through Modulation of Oxidative Stress

Antioxidant Effect of Soymilk Fermented by Lactobacillus plantarum HFY01 on D-Galactose-Induced Premature Aging Mouse Model

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