dc.contributor.author
Radbruch, Helena
dc.contributor.author
Bremer, Daniel
dc.contributor.author
Guenther, Robert
dc.contributor.author
Cseresnyes, Zoltan
dc.contributor.author
Lindquist, Randall
dc.contributor.author
Hauser, Anja E.
dc.contributor.author
Niesner, Raluca
dc.date.accessioned
2018-06-08T03:14:13Z
dc.date.available
2016-04-14T11:20:29.886Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/14754
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-18944
dc.description.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.
en
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject
intravital imaging
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
dc.title
Ongoing Oxidative Stress Causes Subclinical Neuronal Dysfunction in the
Recovery Phase of EAE
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation
Front. Immunol. - 7 (2016), Artikel Nr. 92
dcterms.bibliographicCitation.doi
10.3389/fimmu.2016.00092
dcterms.bibliographicCitation.url
http://dx.doi.org/10.3389/fimmu.2016.00092
refubium.affiliation
Charité - Universitätsmedizin Berlin
de
refubium.mycore.fudocsId
FUDOCS_document_000000024369
refubium.note.author
Der Artikel wurde in einer Open-Access-Zeitschrift publiziert.
refubium.resourceType.isindependentpub
no
refubium.mycore.derivateId
FUDOCS_derivate_000000006281
dcterms.accessRights.openaire
open access