Role of Oxidative Stress in Aβ Animal Model of Alzheimer's Disease: Vicious Circle of Apoptosis, Nitric Oxide and Age

To date, the beta amyloid (Aβ) cascade hypothesis remains the main pathogenetic model of Alzheimer's disease (AD), but its role in the majority of sporadic AD cases is unclear. The “mitochondrial cascade hypothesis” could explain many of the biochemical, genetic, and pathological features of sporadic AD. Somatic mutations in mitochondrial DNA (mtDNA) could cause energy failure, increased oxidative stress, and accumulation of Aβ, which in a vicious cycle reinforce the mtDNA damage and the oxidative stress. Despite the evidence of mitochondrial dysfunction in AD, no causative mutations in the mtDNA have been detected so far. Indeed, results of studies on the role of mtDNA haplogroups in AD are controversial. In this review we discuss the role of the mitochondria, and especially of the mtDNA, in the cascade of events leading to neurodegeneration, dementia, and AD.

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Role of Nuclear Receptor on Regulation of BDNF and Neuroinflammation in Hippocampus of β-Amyloid Animal Model of Alzheimer’s Disease

Neurotoxicity Research ◽

10.1007/s12640-013-9437-9 ◽

2013 ◽

Vol 25 (4) ◽

pp. 335-347 ◽

Cited By ~ 45

Author(s):

Atish Prakash ◽

Anil Kumar

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Animal Model ◽

Nuclear Receptor ◽

Model Of Alzheimer’S Disease ◽

Β Amyloid

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ROLE OF RADIATION AS EFFECTIVE INTERVENTION IN Aβ INDUCED OXIDATIVE STRESS IN ANIMAL MODEL OF ALZHEIMER’S DISEASE

Asian Journal of Pharmaceutical and Clinical Research ◽

10.22159/ajpcr.2018.v12i1.28550 ◽

2019 ◽

Vol 12 (1) ◽

pp. 227

Author(s):

Khan A ◽

Kamal R ◽

Dhawan Dk ◽

Vijayta Dani Chadha

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Animal Model ◽

Antioxidant Defense ◽

Low Dose ◽

Effective Intervention ◽

Aβ Peptide ◽

Model Of Alzheimer’S Disease ◽

X Irradiation

Objective: The present study was undertaken to study the therapeutic effects of low dose fractionated cranial X-irradiation on reducing the amyloid-beta (Aβ) induced oxidative stress burden in an animal model of Alzheimer’s disease (AD).Methods: S.D. female rats received an intracerebroventricular injection of Aβ peptide at stereotaxically defined points. Experimental sessions were conducted by randomly dividing animals into four groups, namely sham-operated, Aβ-injected, and Aβ injection followed by cranial X-irradiation and only cranial X-irradiated. Anesthetized animals received 5 μl synthetic Aβ peptide injection with a 10 μl Hamilton microsyringe with the needle kept in place for a period of 2min following injection. Sham-operated group received 5 μl of bidistilled water instead of Aβ peptide. Animals were treated 6 weeks post-surgery with fractionated radiation of 2Gy for 5 days. Neurobehavior studies were undertaken to confirm memory impairment along with biochemical indices involved in the antioxidant defense system.Results: Fractionated cranial X-irradiation proved effective in restoration of activity of enzymes involved in the antioxidant defense system; the lipid peroxidation and catalase levels that showed a significant increase in Aβ-treated group decreased on subsequent X-irradiation. Moreover, the decrease in the superoxide dismutase, glutathione, glutathione-S-transferase, and glutathione reductase levels witnessed an increase post-irradiation, implicating the X-irradiation to be an effective intervention to restore the redox status of the oxidatively stressed brain cells in AD condition.Conclusion: The present study evaluated the therapeutic potential of low dose fractionated cranial X- irradiation by mitigating the amyloid-induced oxidative stress suggesting a novel treatment for AD-associated pathologies.

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