Pro-oxidant diet enhances β/γ secretase-mediated APP processing in APP/PS1 transgenic mice

Choudhry, Fahd; Howlett, David; Richardson, Jill C.; Francis, Paul T.; Williams, Robert J.

doi:10.1016/j.neurobiolaging.2010.07.008

Cited by 32 publications

(21 citation statements)

References 33 publications

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“…The Nrf2 antioxidant pathway was impaired in transgenic AD mice concomitantly with an increased brain Aβ burden60. Previous work by Choudhry showed a 50% reduction in Nrf2 levels in transgenic AD mice61. The induction of the Nrf2 pathway by small-molecule compounds protects against neuronal oxidative stress and toxicity induced by Aβ in vitro 62.…”

Section: Discussionmentioning

confidence: 91%

Vanillic acid attenuates Aβ1-42-induced oxidative stress and cognitive impairment in mice

Amin

Shah

Kim

2017

Sci Rep

170

115

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Increasing evidence demonstrates that β-amyloid (Aβ) elicits oxidative stress, which contributes to the pathogenesis and disease progression of Alzheimer’s disease (AD). The aims of the present study were to determine and explore the antioxidant nature and potential mechanism of vanillic acid (VA) in Aβ1-42-induced oxidative stress and neuroinflammation mediated cognitive impairment in mice. An intracerebroventricular (i.c.v.) injection of Aβ1-42 into the mouse brain triggered increased reactive oxygen species (ROS) levels, neuroinflammation, synaptic deficits, memory impairment, and neurodegeneration. In contrast, the i.p. (intraperitoneal) administration of VA (30 mg/kg, for 3 weeks) after Aβ1-42-injection enhanced glutathione levels (GSH) and abrogated ROS generation accompanied by an induction of the endogenous nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) via the activation of Akt and glycogen synthase kinase 3β (GSK-3β) in the brain mice. Additionally, VA treatment decreased Aβ1-42-induced neuronal apoptosis and neuroinflammation and improved synaptic and cognitive deficits. Moreover, VA was nontoxic to HT22 cells and increased cell viability after Aβ1-42 exposure. To our knowledge, this study is the first to reveal the neuroprotective effect of VA against Aβ1-42-induced neurotoxicity. Our findings demonstrate that VA could potentially serve as a novel, promising, and accessible neuroprotective agent against progressive neurodegenerative diseases such as AD.

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Section: Discussionmentioning

confidence: 91%

Vanillic acid attenuates Aβ1-42-induced oxidative stress and cognitive impairment in mice

Amin

Shah

Kim

2017

Sci Rep

170

115

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“…This relationship has been shown in human studies and is supported in many mice models [13–16]. Reactivity of ROS can be terminated if the radical meets and reacts with an antioxidant molecule such as vitamins C or E (α-tocopherol), leading to neutralised or greatly reduced reactivity.…”

Section: Introductionmentioning

confidence: 76%

A Critical Review of Vitamin C for the Prevention of Age-Related Cognitive Decline and Alzheimer's Disease

Harrison

2012

JAD

149

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Antioxidants in the diet have long been thought to confer some level of protection against the oxidative damage that is involved in the pathology of Alzheimer’s disease as well as general cognitive decline in normal aging. Nevertheless, support for this hypothesis in the literature is equivocal. In the case of vitamin C (ascorbic acid) in particular, lack of consideration of some of the specific features of vitamin C metabolism has led to studies in which classification of participants according to vitamin C status is inaccurate, and the absence of critical information precludes the drawing of appropriate conclusions. Vitamin C levels in plasma are not always reported, and estimated daily intake from food diaries may not be accurate or reflect actual plasma values. The ability to transport ingested vitamin C from the intestines into blood is limited by the saturable sodium-dependent vitamin C transporter (SVCT1) and thus very high intakes, and the use of supplements are often erroneously considered to be of greater benefit that they really are. The current review documents differences among the studies in terms of vitamin C status of participants. Overall, there is a large body of evidence that maintaining healthy vitamin C levels can have a protective function against age-related cognitive decline and Alzheimer’s disease, but avoiding vitamin C deficiency is likely to be more beneficial than taking supplements on top of a normal, healthy diet.

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“…The experiments were conducted according to the Council of Europe (Directive 86/609) and Danish guidelines. Male transgenic mice and wild-type controls were fed either a modified High Oxidant, Low Antioxidant Diet (TD.06186, Harlan, UK-see Choudhry et al 2010 for details) or control chow from 3 months of age until 6 months when they were humanely killed by cervical dislocation under deep anaesthesia. Following dissection, samples were rapidly frozen in dry ice.…”

Section: Animals and Dietary Conditionsmentioning

confidence: 99%

“…We have previously shown that feeding a transgenic mouse overexpressing mutant APP and presenilin-1 proteins (APPxPS1) with a dietary regimen inducing oxidative stress results in increases in amyloidogenic processing (Choudhry et al 2010). In the present study, we have used a similar dietary regimen, focussing on effects on a range of proteins as markers of synaptic function and oxidative status.…”

Section: Introductionmentioning

confidence: 99%

Synaptic protein expression is regulated by a pro-oxidant diet in APPxPS1 mice

et al. 2011

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Dietary factors may play a role in Alzheimer's disease (AD) pathogenesis. In an effort to recapitulate some of the synaptic protein changes observed in the disease, AD transgenic and wild-type mice were fed either a normal or pro-oxidant diet for 3 months from three months of age. Pro-oxidant diet treatment resulted in altered expression of vesicular glutamate transporter-1 and glutamine synthetase, suggesting changes in glutamatergic synaptic function, and increased expression of urokinase plasminogen activator receptor, possibly reflecting oxidative stress.

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Pro-oxidant diet enhances β/γ secretase-mediated APP processing in APP/PS1 transgenic mice

Cited by 32 publications

References 33 publications

Vanillic acid attenuates Aβ1-42-induced oxidative stress and cognitive impairment in mice

Vanillic acid attenuates Aβ1-42-induced oxidative stress and cognitive impairment in mice

A Critical Review of Vitamin C for the Prevention of Age-Related Cognitive Decline and Alzheimer's Disease

Synaptic protein expression is regulated by a pro-oxidant diet in APPxPS1 mice

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