Neophobia, NQO1 and SIRT1 as premorbid and prodromal indicators of AD in 3xTg-AD mice

Torres–Lista, Virginia; Parrado-Fernández, Cristina; Alvarez-Monton, Ismael; Frontiñán-Rubio, Javier; Durán-Prado, Mario; Peinado, Juan R.; Johansson, Björn; Alcaı́n, Francisco J.; Giménez-Llort, Lydia

doi:10.1016/j.bbr.2014.04.055

Cited by 49 publications

(49 citation statements)

References 25 publications

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“…The transgenic mice also featured elevated Aβ and oxidative stress. Previous studies observed reduced levels of Nrf2 protein and mRNA in the postmortem brain and peripheral blood of AD patients and mouse models (Kanninen et al, ; Ramsey et al, ; Torres‐Lista et al, ). Researchers also reported that the level of Nrf2 increased at 3 months and decreased at 12 months in the brain cortex and the peripheral blood mononuclear cells in 3xTg‐AD mice (Mota et al, ).…”

Section: Discussionmentioning

confidence: 90%

Activation of Nrf2/ARE pathway alleviates the cognitive deficits in PS1V97L‐Tg mouse model of Alzheimer’s disease through modulation of oxidative stress

Tian

Wang

et al. 2018

J of Neuroscience Research

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Oxidative stress refers to an imbalance between oxidative and antioxidative systems due to environmental factors. Although oxidative stress is implicated in the pathogenesis of Alzheimer's disease (AD), its precise role is not yet understood. We aimed to investigate the pathogenic mechanisms of the oxidative stress by using in vitro cultured neurons and in vivo AD models of PS1V97L-transgenic (Tg) mice. Our results showed that when oxidative stress became increasingly evident, the endogenous protective pathway of nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE) decreased in 10-month-old PS1V97L-Tg mice. Activating the Nrf2/ ARE pathway suppressed oxidative stress, decreased amyloid-β (Aβ), and improved the cognitive function of the PS1V97L-Tg mice. In contrast, blocking the Nrf2/ARE pathway augmented oxidative injury and decreased the cell viability of PS1V97L-Tg neurons. Our results highlight the role of the Nrf2/ARE pathway in regulating oxidative stress of the PS1V97L-Tg mice and may indicate a potential therapeutic avenue for AD treatment.

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Section: Discussionmentioning

confidence: 90%

Activation of Nrf2/ARE pathway alleviates the cognitive deficits in PS1V97L‐Tg mouse model of Alzheimer’s disease through modulation of oxidative stress

Tian

Wang

et al. 2018

J of Neuroscience Research

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“…At the protein level, there was a modest but significant increase of GCLC with no change in Keap1, NQO1, or GCLM in the APP/PS1 mice. Studies using the 3xTG model of AD also found a significant increase in NQO1 protein in hippocampus and cortex at 2 months of age, but by 6 months of age, NQO1 levels were actually significantly reduced in hippocampus [75]. Finally, nuclear Nrf2 levels were increased at 3 months and decreased at 15 months in the male cortex but unchanged in the female cortex of 3xTG mice [76].…”

Section: Nrf2 In Alzheimer's Diseasementioning

confidence: 99%

Nrf2—a therapeutic target for the treatment of neurodegenerative diseases

Johnson

2015

Free Radical Biology and Medicine

288

228

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The brain is very sensitive to changes in redox status; thus maintaining redox homeostasis in the brain is critical for the prevention of accumulating oxidative damage. Aging is the primary risk factor for developing neurodegenerative diseases. In addition to age, genetic and environmental risk factors have also been associated with disease development. The primary reactive insults associated with the aging process are a result of oxidative stress (OS) and nitrosative stress (NS). Markers of increased oxidative stress, protein and DNA modification, inflammation, and dysfunctional proteostasis have all been implicated in contributing to the progression of neurodegeneration. The ability of the cell to combat OS/NS and maintain a clearance mechanism for misfolded aggregating proteins determines whether or not it will survive. A critical pathway in this regard is the Nrf2 (nuclear factor erythroid 2-related factor 2)- antioxidant response element (ARE) pathway. Nrf2 activation has been shown to mitigate a number of pathologic mechanisms associated with Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. This review will focus on the role of Nrf2 in these diseases and the potential for Nrf2 activation to mitigate disease progression.

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“…Proteins were extracted with SDS-DTT buffer. The level of SOD2, SOD1, NQO1 and Hif-1a (1:1000 dilution, Santa Cruz Biotechnology) was quantified by western blot as described before [23]. Results are expressed as the mean band intensity vs. actin and normalized to control condition (n = 4).…”

Section: Quantification Of Sod1 Sod2 Nqo1 and Hif-1amentioning

confidence: 99%

Regulation of the oxidative balance with coenzyme Q10 sensitizes human glioblastoma cells to radiation and temozolomide

Frontiñán-Rubio

Santiago-Mora

Nieva-Velasco

et al. 2018

Radiotherapy and Oncology

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Neophobia, NQO1 and SIRT1 as premorbid and prodromal indicators of AD in 3xTg-AD mice

Cited by 49 publications

References 25 publications

Activation of Nrf2/ARE pathway alleviates the cognitive deficits in PS1V97L‐Tg mouse model of Alzheimer’s disease through modulation of oxidative stress

Activation of Nrf2/ARE pathway alleviates the cognitive deficits in PS1V97L‐Tg mouse model of Alzheimer’s disease through modulation of oxidative stress

Nrf2—a therapeutic target for the treatment of neurodegenerative diseases

Regulation of the oxidative balance with coenzyme Q10 sensitizes human glioblastoma cells to radiation and temozolomide

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