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. 2019 Dec 5;16:255. doi: 10.1186/s12974-019-1659-1

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 7. — Exacerbation between G6PD dysfunction and neuroinflammation mediated chronic neurodegeneration. The present study elucidated a pathophysiological role of microglial G6PD in PD neurodegeneration. LPS-induced aberrant upregulation of G6PD promoted cellular oxidative stress and NF-кB activation through increasing NADPH availability to NADPH oxidase. Pharmacological inhibition of G6PD activity or biological knockdown of G6PD attenuated oxidative stress, ameliorated inflammatory response of microglia, and prevented DA neurons from LPS-induced chronic degeneration. G6P, glucose-6-phosphate; G6PD, glucose-6-phosphate dehydrogenase; PPP, pentose phosphate pathway; NADPH, nicotinamideadenine-dinucleotide phosphate; NADP⁺, oxidized form of NADPH; R5P, ribose-5-phosphate; LPS: Lipopolysaccharide; 6-AN, 6-aminonicotinamide; DHEA, dehydroepiandrosterone; O₂⁻, superoxide; H₂O₂, hydrogen peroxide; ROS, reactive oxygen species