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Radbruch H, Bremer D, Guenther R, et al. Ongoing Oxidative Stress Causes Subclinical Neuronal Dysfunction in the Recovery Phase of EAE. Front Immunol. 2016;7:92doi: 10.3389/fimmu.2016.00092.
Radbruch, H., Bremer, D., Guenther, R., Cseresnyes, Z., Lindquist, R., Hauser, A. E., & Niesner, R. (2016). Ongoing Oxidative Stress Causes Subclinical Neuronal Dysfunction in the Recovery Phase of EAE. Frontiers in immunology, 792. https://doi.org/10.3389/fimmu.2016.00092
Radbruch, Helena, et al. "Ongoing Oxidative Stress Causes Subclinical Neuronal Dysfunction in the Recovery Phase of EAE." Frontiers in immunology vol. 7 (2016): 92. doi: https://doi.org/10.3389/fimmu.2016.00092
Radbruch H, Bremer D, Guenther R, Cseresnyes Z, Lindquist R, Hauser AE, Niesner R. Ongoing Oxidative Stress Causes Subclinical Neuronal Dysfunction in the Recovery Phase of EAE. Front Immunol. 2016 Mar 14;7:92. doi: 10.3389/fimmu.2016.00092. eCollection 2016. PMID: 27014271; PMCID: PMC4789534.
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Front Immunol. 2016 Mar 14;7:92. doi: 10.3389/fimmu.2016.00092. eCollection 2016.

Ongoing Oxidative Stress Causes Subclinical Neuronal Dysfunction in the Recovery Phase of EAE.

Frontiers in immunology

Helena Radbruch, Daniel Bremer, Robert Guenther, Zoltan Cseresnyes, Randall Lindquist, Anja E Hauser, Raluca Niesner

Affiliations

  1. Department of Neuropathology, Charité - Universitätsmedizin Berlin , Berlin , Germany.
  2. German Rheumatism Research Center (DRFZ) a Leibniz Institute , Berlin , Germany.
  3. German Rheumatism Research Center (DRFZ) a Leibniz Institute, Berlin, Germany; Immundynamics, Charité - Universiätsmedizin Berlin, Berlin, Germany.

PMID: 27014271 PMCID: PMC4789534 DOI: 10.3389/fimmu.2016.00092

Abstract

Most multiple sclerosis (MS) patients develop over time a secondary progressive disease course, characterized histologically by axonal loss and atrophy. In early phases of the disease, focal inflammatory demyelination leads to functional impairment, but the mechanism of chronic progression in MS is still under debate. Reactive oxygen species generated by invading and resident central nervous system (CNS) macrophages have been implicated in mediating demyelination and axonal damage, but demyelination and neurodegeneration proceed even in the absence of obvious immune cell infiltration, during clinical recovery in chronic MS. Here, we employ intravital NAD(P)H fluorescence lifetime imaging to detect functional NADPH oxidases (NOX1-4, DUOX1, 2) and, thus, to identify the cellular source of oxidative stress in the CNS of mice affected by experimental autoimmune encephalomyelitis (EAE) in the remission phase of the disease. This directly affects neuronal function in vivo, as monitored by cellular calcium levels using intravital FRET-FLIM, providing a possible mechanism of disease progression in MS.

Keywords: EAE/MS; FLIM–FRET; NOX; calcium; intravital imaging

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