NADPH oxidase mediates oxidative stress in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease

By D. Wu, P. Teismann, K. Tieu, M. Vila, V. Jackson-Lewis, H. Ischiropoulos, S. Przedborski. Proceedings of the National Academy of Sciences of the United States of America, 2003

641 citations recorded by the source corpus.

Subfields: Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/98634cbbd8448ed7173e3ecf9e0f57eac7b1d622

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Neurology

1. M. Block
2. P. Whitton
3. Melinda E Lull
4. Jau-Shyong Hong
5. S. Przedborski
6. W. Le
7. Yuanyuan Tang
8. S. Gandhi

In Physiology

1. P. Whitton
2. Melinda E Lull
3. M. Block
4. Yuanyuan Tang
5. W. Le
6. Jau-Shyong Hong
7. S. Gandhi
8. A. Abramov

Citations in the corpus

• Exosomes as Drug Delivery Vehicles for Parkinson’s Disease Therapy (2015, background): “Interesting, empty exosomes also decreased ROS levels in activated macrophages down to the levels of the control non-activated cells, although this effect was less significant than the effect of exoCAT.”
• Myeloperoxidase: friend and foe (2005, background): “NADPH oxidase levels (as measured by the up-regulation of gp91 and p67) are increased in this area of the brain in Parkinson’s disease and in mice treated with 1-methyl4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a model for Parkinson’s disease, and mice deficient in NADPH oxidase have less neuronal ”
• Parkinson's Disease Mechanisms and Models (2003, background): “PD patients striatal terminals prevents the loss of SNpc dopaminergic neurons (Wu et al., 2003).”
• Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases (2015, background): “Similarly, typical characteristics of M1 phenotype including the activation of NADPH oxidase and NF-κB pathways, as well as the release of various pro-inflammatory mediators were observed in the MPTP-intoxicated models [79–81].”
• Inflammation as a causative factor in the aetiology of Parkinson's disease (2007, background): “Activated microglia under the influence of T cells produce ROS (Gao et al., 2003a; Wu et al., 2003), as well as proinflammatory prostaglandins and cytokines, which cause further disease progression (Arai et al., 2004, 2006; Lucas et al., 2006).”
• Microglia-mediated neurotoxicity: uncovering the molecular mechanisms (2007, background): “Some neurotoxins, such as MPTP, require the presence of neurons to induce microglial activation, and effect their damage through direct action on neurons and indirectly by overactivating microgli”
• Microglia and inflammation-mediated neurodegeneration: multiple triggers with a common mechanism. (2005, background): “Further, NADPH oxidase is upregulated in neurodegenerative diseases such as PD (Wu et al., 2003), emphasizing the importance of microglial NADPH oxidase activation for the survival of neurons.”
• Microglial Activation & Chronic Neurodegeneration (2010, background): “Importantly, several studies have shown that microglia have an active role in the process of neuronal death in MPTP/MPP -induced neurotoxicity.(137,140,159) Specifically, in vitro studies show that while MPTP directly damages DA neurons, both MPTP and MPP fail to directly activate microglia.”
• Mechanism of Oxidative Stress in Neurodegeneration (2012, background): “Ubiquitination of a number of substrates by parkin then activates the autophagy of damaged mitochondria.”