Increase of Brain Oxidative Stress in Mild Cognitive Impairment

Praticò, Domenico; Clark, Christopher M.; Liun, Feyan; Lee, Virginia Y.-M.; Trojanowski, John Q.

doi:10.1001/archneur.59.6.972

Cited by 547 publications

(382 citation statements)

References 35 publications

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“…This same result was replicated in additional groups of probable AD patients and controls using both the original method [113][114][115] and the modified method [108], although the latter showed an average increase in LOAD exceeding 200%. In distinction to autopsy studies where tissue oxidative damage markers were equivalent in brains of patients with MCI and LOAD, lumbar CSF F 2 -IsoPs concentrations from MCI patients were intermediate between those from controls and patients with probable AD [116].…”

Section: Biofluid Studiesmentioning

confidence: 57%

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Sonnen¹,

Breitner²,

Lovell³

et al. 2008

Free Radical Biology and Medicine

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Section: Biofluid Studiesmentioning

confidence: 57%

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Sonnen¹,

Breitner²,

Lovell³

et al. 2008

Free Radical Biology and Medicine

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“…The pathophysiology of AD is complex and most likely involves multiple distinct and overlapping pathways of neuronal damage. In addition to the presence of the pathological hallmarks of the disease (senile plaques and neurofibrillary tangles), AD brains exhibit other abnormalities: loss of synapses, gliosis, microglial activation, signs of inflammation and oxidative damage (Pratico et al, 2002b). Current evidence suggests that both oxidative stress and neuroinflammation are early events in the pathogenesis of AD.…”

Section: Conmentioning

confidence: 99%

Aluminum and copper in drinking water enhance inflammatory or oxidative events specifically in the brain

Becaria

Lahiri

Bondy

et al. 2006

Journal of Neuroimmunology

120

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Inflammatory and oxidative events are up-regulated in the brain of AD patients. It has been reported that in animal models of AD, exposure to aluminum (Al) or copper (Cu) enhanced oxidative events and accumulation of amyloid beta (Ah) peptides. The present study was designed to evaluate the effect of a 3-month exposure of mice to copper sulfate (8 AM), aluminum lactate (10 or 100 AM), or a combination of the salts. Results suggest that although Al or Cu may independently initiate inflammatory or oxidative events, they may function cooperatively to increase APP levels. D

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“…In fact, it has been described that oxidative damage is an early event in this pathology and that there is even an increased brain oxidative damage before the appearance of dementia symptoms. 5,6 This oxidative damage occurs due to an imbalance between ROS production and antioxidant cell defenses. 2,7,8 The elevation of oxidative stress actions lead to mitochondrial dysfunction, causing an increase in free radical production and an exacerbation of the oxidative stress cycle.…”

mentioning

confidence: 99%

Mitigation of ROS Insults by Streptomyces Secondary Metabolites in Primary Cortical Neurons

Leirós

Albrecht

Sánchez

et al. 2013

ACS Chem. Neurosci.

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Oxidative stress is a common point in neurodegenerative diseases, widely connected with mitochondrial dysfunction. In this study, we screened seven natural products from Streptomyces sources against hydrogen peroxide insult in primary cortical neurons, an oxidative stress in vitro model. We showed the ability of these compounds to inhibit neuronal cytotoxicity and to reduce ROS release after 12 h treatment. Among the tested compounds, the quinone anhydroexfoliamycin and the red pyrrole-type pigment undecylprodigiosin stand out. These two compounds displayed the most complete protection against oxidative stress with mitochondrial function improvement, ROS production inhibition, and increase of antioxidant enzyme levels, glutathione and catalase. Further investigations confirmed that anhydroexfoliamycin acts over the Nrf2-ARE pathway, as a Nrf2 nuclear translocation inductor, and is able to strongly inhibit the effect of the mitochondrial uncoupler FCCP over cytosolic Ca 2+ , pointing to mitochondria as a cellular target for this molecule. In addition, both compounds were able to reduce caspase-3 activity induced by the apoptotic enhancer staurosporine, but undecylprodigiosin failed to inhibit FCCP effects and it did not act over the Nrf2 pathway as was the case for anhydroexfoliamycin. These results show that Streptomyces metabolites could be useful for the development of new drugs for prevention of neurodegenerative disorders such as Parkinson's and Alzheimer's diseases and cerebral ischemia.

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Increase of Brain Oxidative Stress in Mild Cognitive Impairment

Cited by 547 publications

References 35 publications

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Aluminum and copper in drinking water enhance inflammatory or oxidative events specifically in the brain

Mitigation of ROS Insults by Streptomyces Secondary Metabolites in Primary Cortical Neurons

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