Evaluation of Coenzyme Q as an Antioxidant Strategy for Alzheimer's Disease

Wadsworth, Teri L.; Bishop, J. A.; Pappu, Anuradha S.; Woltjer, Randall L.; Quinn, Joseph F.

doi:10.3233/jad-2008-14210

Cited by 87 publications

(64 citation statements)

References 29 publications

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“…At the same time, the illness is marked by oxidative damage to the brain [43,44]. As this report shows, acetylcholine may facilitate the reduction of UQ to UQH 2 , one of the main mitochondrial antioxidants and a component of novel Alzheimer treatment strategies [44,45]. Although purely speculative at the present point, our results provide with a hypothesis about a possible contribution to the oxidative damage observed in Alzheimer's disease patients.…”

Section: Discussionmentioning

confidence: 40%

Ubiquinone-10 in gold-immobilized lipid membrane structures acts as a sensor for acetylcholine and other tetraalkylammonium cations

Mårtensson

Hernández

2012

Bioelectrochemistry

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This is an accepted version of a paper published in Bioelectrochemistry. This paper has been peer-reviewed but does not include the final publisher proof-corrections or journal pagination.Citation for the published paper: Mårtensson, C., Agmo Hernańdez, V. (2012 AbstractIt is reported that the reduction of ubiquinone incorporated into supported lipid bilayers and into immobilized liposome layers on gold electrodes is kinetically and thermodynamically enhanced by the presence of acetylcholine and tetrabutylammonium (TBA + ) in solution. The reduction peak and the mid-peak potentials of the redox reactions, determined by cyclic voltammetry, are displaced towards more positive potentials by approximately 500 and 250 mV, respectively, in the case of TBA + ; and by approximately 750 and 530 mV, respectively, in the case of acetylcholine. The intensity of the signal varies with the cation concentration, allowing for quantitative determinations in the millimolar range. It is proposed that the enhanced reduction of ubiquinone arises from the formation of tetraalkylammonium cationubiquinone radical anion ion-pairs. Electrochemical quartz crystal microbalance with dissipation monitoring (EQCM-D) measurements confirmed that the potential shift and the intensity of the redox signal are coupled with the adsorption of the tetraalkylammonium cations on the lipid membrane. The Langmuir adsorption equilibrium constant (K) of TBA + on lipid membranes at physiological pH is determined. In supported lipid bilayers K = 440.7 ± 160 M -1 , while in an immobilized liposome layer K = 35.53 ± 3.53 M -1 . 1

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Section: Discussionmentioning

confidence: 40%

Ubiquinone-10 in gold-immobilized lipid membrane structures acts as a sensor for acetylcholine and other tetraalkylammonium cations

Mårtensson

Hernández

2012

Bioelectrochemistry

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“…We and others have shown that psoriasin is secreted from epithelial cells [9,20]. We hypothesized that psoriasin secreted from mammary epithelial cells may lead to endothelial cell proliferation.…”

Section: Extracellularly Administered Psoriasin Triggers Proliferatiomentioning

confidence: 99%

“…A NBT assay (Sigma-Aldrich, N5514) was performed as previously described [20]. The absorbance was measured at 630 nm using the Mithras LB940 instrument (Berthold Technologies).…”

Section: Nitroblue Tetrazolium (Nbt) Assay For the Detection Of Rosmentioning

confidence: 99%

Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Shubbar

Vegfors

Carlström

et al. 2011

Breast Cancer Res Treat

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Psoriasin (S100A7), originally identified in psoriasis, is a calcium-binding protein belonging to the multigenic S100 family. In high-grade ductal carcinoma in situ (DCIS), psoriasin was identified as one of the most abundant transcripts. We have previously shown that psoriasin was induced by reactive oxygen species (ROS). Moreover, the downregulation of psoriasin by short hairpin RNA (shRNA) led to the reduced expression of VEGF and inhibited tumour Our data suggest that psoriasin expression in mammary epithelial cells leads to increased endothelial cell proliferation in a paracrine manner through RAGE. Psoriasin may therefore play a role in breast cancer progression by promoting oxidative stress response and angiogenesis.

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“…The antioxidants are potential therapeutics by eliminating ROS and exerting neuroprotective effects on neurons in AD properties both in vitro and in vivo [113] ; its administration to transgenic AD mice also dramatically reduces the amyloid plaque burden [114,115] . Although CoQ10 has not been tested in clinic trials, its analog, idebenone, has been assessed in AD patients, and has beneficial effects on memory and attention [116,117] .…”

Section: Antioxidants As a Treatment For Alzheimer's Diseasementioning

confidence: 99%

Oxidative stress in Alzheimer’s disease

2014

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Oxidative stress plays a significant role in the pathogenesis of Alzheimer's disease (AD), a devastating disease of the elderly. The brain is more vulnerable than other organs to oxidative stress, and most of the components of neurons (lipids, proteins, and nucleic acids) can be oxidized in AD due to mitochondrial dysfunction, increased metal levels, infl ammation, and β-amyloid (Aβ) peptides. Oxidative stress participates in the development of AD by promoting Aβ deposition, tau hyperphosphorylation, and the subsequent loss of synapses and neurons. The relationship between oxidative stress and AD suggests that oxidative stress is an essential part of the pathological process, and antioxidants may be useful for AD treatment.Keywords: Alzheimer's disease; oxidative stress; β-amyloid; tau; metals; antioxidants ·Review· IntroductionThe human brain, although it constitutes only 2% of the body weight, consumes ~20% of the oxygen supplied by the respiratory system [1] . The high energy-consumption of the brain means that it is more susceptible to oxidative stress than any other organ. As the basic functional unit of the brain, the neuron is particularly vulnerable to oxidative damage because it has a higher metabolic rate than other cells [2] . The oxidation of lipids, proteins, and nucleic acids in neurons is a common pathological feature of Alzheimer's disease (AD) [3] . Neurons contain a large amount of polyunsaturated fatty acids (PUFAs) that can interact with reactive oxygen species (ROS), leading to a selfpropagating cascade of lipid peroxidation and molecular destruction [4] . Furthermore, neurons contain low levels of glutathione, an essential antioxidant for eliminating free radicals [5] . Therefore, neurons are highly susceptible to oxidative stress.An increased oxidative burden has been reported in the brains of non-demented elderly and/or sporadic AD patients [6,7] . Increased levels of oxidative stress biomarkers in the blood reflect such stress in the brain [8,9] . Currently, many blood markers of oxidative stress have been identified in AD patients or related animal models, including protein carbonyls and 3-nitrotyrosine [10,11] , , malondialdehyde (MDA) [12] , 4-hydroxynonenal (4-HNE), and F2-isoprostanes (F2-IsoPs) [13][14][15][16] . Apart from the intracellular accumulation of free radicals, changes in the activities or expressions of antioxidant enzymes, such as superoxide dismutase (SOD) and catalase, have also been described in both the central nervous system and peripheral tissues of AD patients [14,17] . Thus, oxidative stress is an important pathological feature in AD.However, how and where the oxidative stress originates in AD are open questions. Research has suggested that mitochondrial dysfunction [12,18,19] , metal accumulation [12,20,21] , hyperphosphorylated tau [22,23] , inflammation [24,25] , and β-amyloid (Aβ) accumulation [12,19] are the basic mechanisms underlying the induction of oxidative stress. Deficiency or destruction of components of the antioxidant system such as SOD in the mi...

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Evaluation of Coenzyme Q as an Antioxidant Strategy for Alzheimer's Disease

Cited by 87 publications

References 29 publications

Ubiquinone-10 in gold-immobilized lipid membrane structures acts as a sensor for acetylcholine and other tetraalkylammonium cations

Ubiquinone-10 in gold-immobilized lipid membrane structures acts as a sensor for acetylcholine and other tetraalkylammonium cations

Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Oxidative stress in Alzheimer’s disease

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