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Persistent increase of Nogo-A-positive cells and dynamic reduction in oligodendroglia lineage cells in white matter regions following experimental and clinical traumatic brain injury

Ruscher, Karsten LU ; Michalettos, Georgios LU ; Abu Hamdeh, Sami ; Clausen, Fredrik LU ; Nolan, Amber L. ; Flygt, Johanna ; Özen, Ilknur LU and Marklund, Niklas LU orcid (2025) In Journal of Neuropathology and Experimental Neurology 84(5). p.423-435
Abstract

White matter (WM) disruption and atrophy is a consequence of traumatic brain injury (TBI) and contributes to persisting cognitive impairment. An increased expression of the myelin-associated axonal outgrowth inhibitor Nogo-A and oligodendrocyte pathology might be negatively associated with postinjury WM changes. Here, we analyzed brain tissue from severe TBI patients, obtained by surgical decompression in the early postinjury phase and postmortem brain tissue of long-term TBI survivors and observed an increased number of Nogo-A+ cells in WM tracts such as the corpus callosum (CC). Likewise, the number of Nogo-A+ cells in the CC was increased from day 7 postinjury to 6 months postinjury (mpi) following central fluid... (More)

White matter (WM) disruption and atrophy is a consequence of traumatic brain injury (TBI) and contributes to persisting cognitive impairment. An increased expression of the myelin-associated axonal outgrowth inhibitor Nogo-A and oligodendrocyte pathology might be negatively associated with postinjury WM changes. Here, we analyzed brain tissue from severe TBI patients, obtained by surgical decompression in the early postinjury phase and postmortem brain tissue of long-term TBI survivors and observed an increased number of Nogo-A+ cells in WM tracts such as the corpus callosum (CC). Likewise, the number of Nogo-A+ cells in the CC was increased from day 7 postinjury to 6 months postinjury (mpi) following central fluid percussion injury (cFPI) in mice. In addition, the number of Olig2+ cells in the CC and capsula externa remained constant, while the numbers of Olig2+/CC1+ and GST-π+ mature oligodendrocytes declined throughout the observation time of 18 months. A significantly lower number of Olig2+/CC1+ cells was found in cFPI mice compared to controls at 18 mpi. Persistent vulnerability of oligodendrocytes in combination with dynamic alterations of Nogo-A expression may have implications for the WM atrophy and insufficient recovery observed after TBI.

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author
; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
central fluid percussion injury, long-term recovery, Nogo-A, oligodendrocyte, traumatic brain injury
in
Journal of Neuropathology and Experimental Neurology
volume
84
issue
5
pages
13 pages
publisher
American Association of Neuropathologists
external identifiers
  • scopus:105003481532
  • pmid:40085014
ISSN
0022-3069
DOI
10.1093/jnen/nlaf017
language
English
LU publication?
yes
id
7ce469e0-159f-4efe-898d-aaa91e3753a1
date added to LUP
2025-08-05 11:06:50
date last changed
2025-08-19 12:22:24
@article{7ce469e0-159f-4efe-898d-aaa91e3753a1,
  abstract     = {{<p>White matter (WM) disruption and atrophy is a consequence of traumatic brain injury (TBI) and contributes to persisting cognitive impairment. An increased expression of the myelin-associated axonal outgrowth inhibitor Nogo-A and oligodendrocyte pathology might be negatively associated with postinjury WM changes. Here, we analyzed brain tissue from severe TBI patients, obtained by surgical decompression in the early postinjury phase and postmortem brain tissue of long-term TBI survivors and observed an increased number of Nogo-A<sup>+</sup> cells in WM tracts such as the corpus callosum (CC). Likewise, the number of Nogo-A<sup>+</sup> cells in the CC was increased from day 7 postinjury to 6 months postinjury (mpi) following central fluid percussion injury (cFPI) in mice. In addition, the number of Olig2<sup>+</sup> cells in the CC and capsula externa remained constant, while the numbers of Olig2<sup>+</sup>/CC1<sup>+</sup> and GST-π<sup>+</sup> mature oligodendrocytes declined throughout the observation time of 18 months. A significantly lower number of Olig2<sup>+</sup>/CC1<sup>+</sup> cells was found in cFPI mice compared to controls at 18 mpi. Persistent vulnerability of oligodendrocytes in combination with dynamic alterations of Nogo-A expression may have implications for the WM atrophy and insufficient recovery observed after TBI.</p>}},
  author       = {{Ruscher, Karsten and Michalettos, Georgios and Abu Hamdeh, Sami and Clausen, Fredrik and Nolan, Amber L. and Flygt, Johanna and Özen, Ilknur and Marklund, Niklas}},
  issn         = {{0022-3069}},
  keywords     = {{central fluid percussion injury; long-term recovery; Nogo-A; oligodendrocyte; traumatic brain injury}},
  language     = {{eng}},
  number       = {{5}},
  pages        = {{423--435}},
  publisher    = {{American Association of Neuropathologists}},
  series       = {{Journal of Neuropathology and Experimental Neurology}},
  title        = {{Persistent increase of Nogo-A-positive cells and dynamic reduction in oligodendroglia lineage cells in white matter regions following experimental and clinical traumatic brain injury}},
  url          = {{http://dx.doi.org/10.1093/jnen/nlaf017}},
  doi          = {{10.1093/jnen/nlaf017}},
  volume       = {{84}},
  year         = {{2025}},
}