Natural Antioxidants Protect Neurons in Alzheimer’s Disease and Parkinson’s Disease

Zhao, Baolu

doi:10.1007/s11064-008-9900-9

Cited by 166 publications

(97 citation statements)

References 60 publications

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“…This is especially true for the polyphenol EGCG, which is a potent antioxidant that can also complex iron and copper ions and thus neutralize their catalytic effects in the production of ROS. The mechanisms involved in this activity have been described extensively elsewhere [41,49,50] .…”

Section: Strategies For Intervention Into the Amyloid Formation Cascadementioning

confidence: 99%

Natural Compounds May Open New Routes to Treatment of Amyloid Diseases

Bieschke

2013

Neurotherapeutics

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Protein misfolding disorders, such as Alzheimer's disease and Parkinson's disease, have in common that a protein accumulates in an insoluble form in the affected tissue. The process of aggregation follows a mechanism of seeded polymerization. Although the toxic species is still not well defined, the process, rather than the end product, of fibril formation is likely the main culprit in amyloid toxicity. These findings suggest that therapeutic strategies directed against the protein misfolding cascade should focus on depleting aggregation intermediates rather than on large fibrillar aggregates. Recent studies involving natural compounds have suggested new intervention strategies. The polyphenol epi-gallocatechine-3-gallate (EGCG), the main polyphenol in Camilla sinensis, binds directly to a large number of proteins that are involved in protein misfolding diseases and inhibits their fibrillization. Instead, it promotes the formation of stable, spherical aggregates. These spherical aggregates are not cytotoxic, have a lower β-sheet content than fibrils, and do not catalyze fibril formation. Correspondingly, epi-gallocatechine-3-gallate remodels amyloid fibrils into aggregates with the same properties. Derivatives of Orcein, which is a phenoxazine dye that can be isolated from the lichen Roccella tinctoria, form a second promising class of natural compounds. They accelerate fibril formation of the Alzheimer's disease-related amyloid-beta peptide. At the same time these compounds deplete oligomeric and protofibrillar forms of the peptide. These compounds may serve as proof-of-principle for the strategies of promoting and redirecting fibril formation. Both may emerge as two promising new therapeutic approaches to intervening into protein misfolding processes.

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Section: Strategies For Intervention Into the Amyloid Formation Cascadementioning

confidence: 99%

Natural Compounds May Open New Routes to Treatment of Amyloid Diseases

Bieschke

2013

Neurotherapeutics

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“…Thus, green tea consumption may also show potential preventive effects against several oxidative stress-related disorders such as cardiovascular diseases (Rickman et al, 2010;Plutner et al, 1990;Nantz et al, 2009) and several types of cancer such as breast, prostate, lung, skin, gastric and colon cancer. It also shows neuroprotective effects in Parkinson and Alzeimer's disease (Zhao, 2009), ameliorates several autoimmune diseases such as autoimmune arthritis (Kim, H. R. et al, 2008), and immune-mediated liver injury (Wang et al, 2006) or even it seems to prevent skin cell damage (Jorge et al 2011). Furthermore, green tea (or its active biomolecule EGCG) could be one potential anti-obesogenic agent (Stefanovic et al, 2008) and might be used in the prevention and treatment of this disease.…”

Section: Green Teamentioning

confidence: 99%

Compounds with Antioxidant Capacity as Potential Tools Against Several Oxidative Stress Related Disorders: Fact or Artifact?

Pérez-Matute¹,

Crujeiras²,

Fernández‐Galilea³

et al. 2012

Oxidative Stress and Diseases

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Oxidative Stress and Diseases 544 reactive species: reactive oxygen species (ROS, thus, oxygen-containing molecules that are highly reactive), reactive chlorine species (RCN) and reactive nitrogen species (RNS). All these reactants contain free radicals as well as nonradicals. Low concentrations of these reactive species are necessary for normal cell redox status, cell function and intracellular signalling (Droge, 2002;Valko et al., 2007;Perez-Matute et al., 2009). However, in some disease states, free radicals are produced in excess and can damage DNA, proteins, carbohydrates and lipid constituents and compromise cell function leading to the development of type 2 diabetes, atherosclerosis, obesity, arthritis etc. Thus, it is clear that excessive production of free radicals causes damage to biological material and is an essential event in the aetiopathogenesis of various diseases. However, the question that has risen in the past years is whether uncontrolled formation of ROS is a primary cause or a downstream consequence of the pathological processes. In other words, it is still not clear what comes first, the chicken or the egg. However, what is clear is that there must be a balance between these reactive species and the antioxidants, whose main function is to counteract the deleterious effects of these reactive species. In fact, antioxidant is defined as any substance that when present at low concentrations compared with those of an oxidizable substrate, significantly delays or prevents oxidation of that substrate (Halliwell & Gutteridge, 1999). These defences include both enzymatic (superoxide dismutases, glutathione peroxidase, catalase, thioredoxin) and non-enzimatic systems (vitamins such as vitamin C, E, A, minerals such as selenium, zinc, cooper, bilirrubine, uric acid, some aminoacids etc).Several studies have demonstrated an increased oxidative state (either caused by an increased ROS production or diminished levels of antioxidants) in serious pathologies such as obesity, cardiovascular diseases, metabolic syndrome, cancer etc. Thus, oxidative stress actually may be related with the mentioned processes. In this context, it is tempting to suggest that if oxidative damage significantly contributes to disease pathology, then, actions that decrease it (via decreasing ROS production or increasing endogenous levels of antioxidants) might be therapeutically beneficial. In fact, attenuation or complete suppression of oxidative stress as a way to improve several diseases has flourished as one of the main challenges of research in the last years. Thus, several approaches have been carried out in order to either decrease the high levels of ROS generated or boost the endogenous levels of antioxiants. Inhibition of ROS production through the development of inhibitors (natural or chemical) against the main sources of ROS generation offers an interesting approach. Thus, NADPH oxidase and mitochondria have been postulated as the main targets to reduce ROS production (reviewed by Pérez-Matute et al., 2009). Another str...

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“…As the major component of ROS, hydrogen peroxide (H 2 O 2 ) is generally used as an inducer of oxidative stress in vitro models by many laboratories (Tabner et al, 2002;Zhang et al, 2007;Bi et al, 2008). Some compounds have been proven to possess neuroprotective potential as antioxidants, such as curcumin, resveratrol, lipoic acid, (−)-epigallocatechin-3-gallate (EGCG), and melatonin (Mecocci et al, 2008;Zhao, 2009 (Zhou et al, 2005). Recently, SM and its active ingredients have attracted increasing attention for the treatment of neurodegenerative diseases.…”

Section: Research Articlementioning

confidence: 99%