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Urate as a Marker of Risk and Progression of Neurodegenerative Disease.

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TLDR
A body of evidence supports the hypothesis that urate may represent a shared pathophysiologic mechanism across neurodegenerative diseases and suggests that it may constitute a novel therapeutic target.
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This article is published in Neurotherapeutics.The article was published on 2017-01-01 and is currently open access. It has received 72 citations till now. The article focuses on the topics: Neurodegeneration.

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Physiology of Hyperuricemia and Urate-Lowering Treatments.

TL;DR: This work discusses current therapies and emerging drug discovery efforts aimed at delivering an optimized clinical treatment strategy for gout, with a focus on studies which suggest association of hyperuricemia with common comorbidities including cardiovascular disease, renal insufficiency, metabolic syndrome and diabetes.
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Formate metabolism in health and disease.

TL;DR: The relevance of formate metabolism in the context of embryonic development, cancer, obesity, immunometabolism, and neurodegeneration is discussed, along with an outlook of some open questions bringing formates metabolism into the spotlight.
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Oxidative stress in cerebral small vessel disease. Role of reactive species.

TL;DR: Cerebral small vessel disease is a wide term describing the condition affecting perforating arterial branches as well as arterioles, venules, and capillaries, which can be caused by oxidative stress and inflammatory mechanisms as a result of reactions and processes generating extensive reactive oxygen species (ROS) production.
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Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis.

TL;DR: It is shown that, at physiological concentrations, urate reduces the oxo-heme oxidant formed by peroxide reaction with hemoglobin, protects erythrocyte ghosts against lipid peroxidation, and protects ERYthrocytes from peroxidative damage leading to lysis.
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Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis

TL;DR: Evidence for the roles of mitochondrial dysfunction and increased oxidative stress in the neuronal loss that leads to PD is examined and how this knowledge might further improve patient management and aid in the development of 'mitochondrial therapy' for PD is discussed.
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Dietary folate deficiency and elevated homocysteine levels endanger dopaminergic neurons in models of Parkinson's disease

TL;DR: The ability of folate deficiency and elevated homocysteine levels to sensitize dopaminergic neurons to environmental toxins suggests a mechanism whereby dietary folate may influence risk for PD.
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Metabolomic profiling to develop blood biomarkers for Parkinson's disease.

TL;DR: In this article, the authors used metabolomic profiling using high performance liquid chromatography coupled with electrochemical coulometric array detection (LCECA) to look for biomarkers in plasma useful for the diagnosis of Parkinson's disease.
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