The therapeutic potential of monoamine oxidase inhibitors
By M. Youdim, D. Edmondson, K. Tipton. Nature Reviews Neuroscience, 2006
1,300 citations recorded by the source corpus.
Subfields: Biological Psychiatry, Cellular and Molecular Neuroscience, Neurology
View Paper: https://www.semanticscholar.org/paper/75df674403d78e9badf4fe892aee17bd9ea36a6b
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In Cellular and Molecular Neuroscience
In Neurology
Citations in the corpus
- 13 reasons why the brain is susceptible to oxidative stress (2018, background): “line, MOA-A preferentially metabolises 5-hydroxytryptamine whereas MOA-B prefers 2-phenylethylamine [124,125].”
- The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “However, with neuronal degeneration that occurs in PD and aging, MAO-B located in glial cells increases and becomes the predominant enzyme to metabolize dopamine [50–52], which is taken up by astrocytes via sodium-dependent and independent mechanisms [53–55].”
- The Link between Depression and Chronic Pain: Neural Mechanisms in the Brain (2017, background): “Because clinical depression is associated with a decreased system of NE and/or 5-HT content in some regions of the CNS, the antidepressant effect of the classical monoamine oxidase inhibitor (MAOI) might be related to its ability to increase the NE and/or 5-HT levels of these sites [21, 85].”
- Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome. (2015, neutral): “, 2002), possibly because dopamine can be broken down into inactive metabolites by a set of enzymes, such as monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT) (Youdim et al., 2006).”