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Strategy to reduce free radical species in Alzheimer's disease: an update of selected antioxidants.

Expert review of neurotherapeutics (2014-09-23)
Fabio Di Domenico, Eugenio Barone, Marzia Perluigi, D Allan Butterfield
RESUMEN

Alzheimer's disease (AD), characterized by progressive loss of memory, language, reasoning and other cognitive functions, including dementia, is characterized pathologically by the presence of senile plaques, neurofibrillary tangles and synapse loss. Increased oxidative/nitrosative stress, decreased antioxidants, mitochondrial damage and other factors play major roles in the development and progression of AD. Strategies to reduce pro-oxidant species to ameliorate AD pathology have been proposed with mixed results. In this review, we focus on the most recent in vitro and in vivo antioxidant approaches for removing oxidant species with relevance to AD, including N-acetyl-l-cysteine, vitamin D, vitamin E, ferulic acid, tricyclodecan-9-yl-xanthogenate, selenium and melatonin as therapeutic stratagems in AD management. In addition, we reviewed the most effective mitochondria targeted antioxidants such as coenzyme Q10 and lipoic acid. We suggest the use of multitargeted approaches by formulas containing one or more antioxidant compounds may be more promising than single-agent approaches.

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Sigma-Aldrich
L-Glutationa oxidada, ≥98% (HPLC)
Sigma-Aldrich
L-Glutatión reducido, suitable for cell culture, BioReagent, ≥98.0%, powder
Sigma-Aldrich
L-Glutatión reducido, ≥98.0%
Sigma-Aldrich
L-Glutationa oxidada, lyophilized powder
Supelco
L-Glutatión reducido, Pharmaceutical Secondary Standard; Certified Reference Material
Sigma-Aldrich
L-Glutationa oxidada, BioXtra, ≥98%
SAFC
L-Glutationa oxidada
Sigma-Aldrich
L-Glutatión reducido, BioXtra, ≥98.0%
L-Glutatión reducido, European Pharmacopoeia (EP) Reference Standard