Preventive Effect of Grape Seed Hydroalcholic Extract on Dementia Type of Alzheimer's Disease in Aged Male Rats

2009 ◽  
Vol 5 (4) ◽  
pp. 257-262 ◽  
Author(s):  
Farbood Y. ◽  
Sarkaki A. ◽  
Badavi M.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Grape Seed ◽  
Male Rats ◽  
Preventive Effect

scholarly journals ANTINEURODEGENERATIVE ACTIVITY OF MICROALGAE DUNALIELLA SALINA IN RATS WITH ALZHEIMER’S DISEASE

2016 ◽  
Vol 10 (1) ◽  
pp. 134 ◽  
Author(s):  
Farouk Kamel Elbaz ◽  
Hanan F Aly ◽  
Wagdy Kb Khalil ◽  
Hoda F Booles ◽  
Gamila H Al
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurotrophic Factor ◽  
Dunaliella Salina ◽  
Brain Derived Neurotrophic Factor ◽  
Male Rats ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
The Brain ◽  
Antioxidant Effects

ABSTRACTObjective: The present study is aimed to investigate the promising action of Dunaliella salina extract as a natural protector against Alzheimer’sdisease (AD) and reported to possess a variety of activities, including antioxidant effects due to its ability to create large amount of carotenoids.Methods: D. salina is a type of halophile green microalgae was used in the present study. 50 male rats were used in this study, where aluminumchloride was orally administered to induce AD in a dose of 100 mg/kg, daily for 6 weeks. Al-intoxicated rats treated orally daily with D. salinaethanolic extract for 6 weeks in a dose of 150 mg/kg b.wt., whereas standard anti-Alzheimer drug donepezil tartrate was administered at the doseof 10 mg/kg b.wt./day for 6 consecutive weeks. The anti-Alzheimer properties of D. salina extract were achieved through measuring the calmodulin(CaM) level, paraoxonase 1 (PON1) activity, the antiapoptotic marker (Bcl2), brain-derived neurotrophic factor (BDNF), the generation of the DNAadducts (8-hydroxy-2-deoxyguanosine [8-OHdG]/2-deoxy guanosine [2-dG]), and alteration in the expression of amyloid precursor protein, β-siteAPP-cleaving enzyme 1 (BACE1), and β-site APP-cleaving enzyme 2 (BACE2) in AD rats.Results: The current results demonstrated that supplementation of AD rats with D. salina extract-enhanced CaM level, and increased PON1 activity,upregulated Bcl2 and BDNF, decreased the levels of DNA adducts (8-OHdG/2-dG), and suppressed the alterations of the expression levels of APP,BACE1, and BACE2-m RNAs as compared with those in AD rats.Conclusion: It could be concluded that the biological activity of D. salina extract might be regulated by 9-cis b-carotene protecting the brain cells fromthe oxidative stress in AD rats.Keywords: Dunaliella salina, Calmodulin, Paraoxonase 1, Bcl2, Brain-derived neurotrophic factor, Alzheimer’s disease, DNA adduct, Amyloid precursorprotein.

scholarly journals Dietary vitamin E, brain redox status and expression of Alzheimer's disease-relevant genes in rats

2009 ◽  
Vol 102 (3) ◽  
pp. 398-406 ◽  
Author(s):  
Sonja Gaedicke ◽  
Xiangnan Zhang ◽  
Patricia Huebbe ◽  
Christine Boesch-Saadatmandi ◽  
Yijia Lou ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin E ◽  
Adverse Effects ◽  
Redox Status ◽  
Male Rats ◽  
Dietary Vitamin ◽  
Beneficial Effects ◽  
Positive Effects ◽  
Total Superoxide Dismutase

Oxidative stress is one of the major pathological features of Alzheimer's disease (AD). Here, we investigated whether dietary vitamin E (VE) depletion may induce adverse effects and supplementation with α-tocopherol (αT) may result in beneficial effects on redox status and the regulation of genes relevant in the pathogenesis of AD in healthy rats. Three groups of eight male rats each were fed diets with deficient ( < 1 mg αT equivalents/kg diet), marginal (9 mg αT equivalents/kg diet) or sufficient (18 mg αT equivalents/kg diet) concentrations of natural-source VE for 6 months; a fourth group was fed the VE-sufficient diet fortified with αT (total VE, 146 mg αT equivalents/kg diet). Feeding of the experimental diets dose dependently altered αT concentrations in the cortex and plasma. No significant changes in F2-isoprostane concentrations, activities of antioxidative enzymes (total superoxide dismutase, Se-dependent glutathione peroxidase) and concentrations of glutathione or the expression of AD-relevant genes were observed. In this non-AD model, depletion of VE did not induce adverse effects and supplementation of αT did not induce positive effects on the parameters related to the progression of AD.

scholarly journals Effects of grape seed proanthocyanidin on Alzheimer's disease in vitro and in vivo

2016 ◽  
Vol 12 (3) ◽  
pp. 1681-1692 ◽  
Author(s):  
Qingwang Lian ◽  
Yongsheng Nie ◽  
Xiaoyou Zhang ◽  
Bo Tan ◽  
Hongying Cao ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Grape Seed ◽  
Grape Seed Proanthocyanidin

Anti‐Alzheimer's disease potential of Arabian coffee versus Date palm seed extract in male rats

2021 ◽  
Author(s):  
Nahla S. Zidan ◽  
Awatif M. E. Omran ◽  
Samar M. Rezk ◽  
Hebatallah H. Atteia ◽  
Mohamed I. Sakran
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Date Palm ◽  
Seed Extract ◽  
Male Rats

scholarly journals Enduring glucocorticoid-evoked exacerbation of synaptic plasticity disruption in male rats modelling early Alzheimer’s disease amyloidosis

2021 ◽  
Author(s):  
Yingjie Qi ◽  
Igor Klyubin ◽  
Tomas Ondrejcak ◽  
Neng-Wei Hu ◽  
Michael J. Rowan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Transgenic Animals ◽  
Long Term Potentiation ◽  
Male Rats ◽  
Model Of Alzheimer’S Disease ◽  
Term Potentiation ◽  
Early Alzheimer’S Disease

AbstractSynaptic dysfunction is a likely proximate cause of subtle cognitive impairment in early Alzheimer’s disease. Soluble oligomers are the most synaptotoxic forms of amyloid ß-protein (Aß) and mediate synaptic plasticity disruption in Alzheimer’s disease amyloidosis. Because the presence and extent of cortisol excess in prodromal Alzheimer’s disease predicts the onset of cognitive symptoms we hypothesised that corticosteroids would exacerbate the inhibition of hippocampal synaptic long-term potentiation in a rat model of Alzheimer’s disease amyloidosis. In a longitudinal experimental design using freely behaving pre-plaque McGill-R-Thy1-APP male rats, three injections of corticosterone or the glucocorticoid methylprednisolone profoundly disrupted long-term potentiation induced by strong conditioning stimulation for at least 2 months. The same treatments had a transient or no detectible detrimental effect on synaptic plasticity in wild-type littermates. Moreover, corticosterone-mediated cognitive dysfunction, as assessed in a novel object recognition test, was more persistent in the transgenic animals. Evidence for the involvement of pro-inflammatory mechanisms was provided by the ability of the selective the NOD-leucine rich repeat and pyrin containing protein 3 (NLRP3) inflammasome inhibitor Mcc950 to reverse the synaptic plasticity deficit in corticosterone-treated transgenic animals. The marked prolongation of the synaptic plasticity disrupting effects of brief corticosteroid excess substantiates a causal role for hypothalamic-pituitary-adrenal axis dysregulation in early Alzheimer’s disease.

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