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Cited by 76Multiple Sclerosis Research StudiesNeuroinflammation and Neurodegeneration MechanismsPeripheral Neuropathies and Disorders

Molecular changes in white matter adjacent to an active demyelinating lesion in early multiple sclerosis.

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Zeis, Thomas, Probst, Alfonse, Steck, Andreas Johann, Stadelmann, Christine, Brück, Wolfgang, Schaeren‐Wiemers, Nicole·2009·Brain Pathology
DOI 10.1111/j.1750-3639.2008.00231.xPMC PMC8094783
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Abstract

A stereotactic biopsy of a 17-year-old woman revealed an active inflammatory demyelinating lesion compatible with pattern III multiple sclerosis (MS) according to Lucchinetti et al. The biopsy included a white matter region distant from the active inflammatory demyelinating lesion with abnormal MRI signal, lacking histopathological signs of demyelination and/or oligodendrocyte apoptosis. Expression analysis of this area revealed a strong up-regulation of neuronal nitric oxide synthase (nNOS). Furthermore, detection of nitrotyrosine provided evidence for reactive nitrogen species (RNS)-mediated damage to oligodendrocytes. Concomitantly, genes involved in neuroprotection against oxidative stress such as heme oxygenase 1 were up-regulated. Even though a single case report, this study shows earliest molecular changes in white matter surrounding an actively demyelinating lesion during the first manifestation of MS, pointing toward a more widespread pathological process. Therapeutic targeting of the identified mechanisms of tissue injury might be crucial to prevent further lesion formation or secondary tissue damage.

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Crossref · 10.1111/j.1750-3639.2008.00231.x

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  • Multiple sclerosis attack disrupts the blood-brain barrier in the section of brain or spinal cord from where peripheral T lymphocytes gain access to the brain and attack myelin gradually, leading to demyelination.

    “MS attack disrupt BBB in the section of brain or spinal cord from where peripheral T lymphocytes gain access to brain and attack the myelin gradually leading to demyelination”

    From Nanotechnology: A Promising Approach for Delivery of Neuroprotective Drugs (2020) · cites this paper as Zeis et al., 2009

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Authors
Zeis, T., Probst, A., Steck, A. J., Stadelmann, C., Brück, W., & Schaeren‐Wiemers, N.
Affiliations
  • University Hospital of Basel (CH)
  • University of Göttingen (DE)
ORCID
Venue
Brain Pathology
Publisher
Wiley
Published
2009-06-10
Volume
19
Issue
3
Pages
459-466
ISSN
  • 1015-6305 (ISSN-L)
  • 1750-3639
DOI
10.1111/j.1750-3639.2008.00231.x
PMC
PMC8094783
OpenAlex
W1994629901
Cited by
76
References
32
Citations by year
2026: 1 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 3 · 2019: 1 · 2018: 4 · 2017: 5 · 2016: 2 · 2015: 6 · 2014: 8 · 2013: 12 · 2012: 10
FWCI
5.64
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Brain Pathology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • GRO (submittedVersion)
Funders
Georg-August-Universität Göttingen
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Neurology › Peripheral Neuropathies and Disorders
Keywords
multiple sclerosis, demyelination, white matter, neuronal nitric oxide synthase, nitrotyrosine, reactive nitrogen species, oligodendrocyte damage, heme oxygenase-1, oxidative stress, neuroprotection, early-stage disease, stereotactic biopsy, gene expression
MeSH terms
Adolescent, Adult, Aged, Brain, Demyelinating Diseases, Female, Humans, Inflammation, Magnetic Resonance Imaging, Male, Middle Aged, Multiple Sclerosis, Up-Regulation, Gene Expression, Reverse Transcriptase Polymerase Chain Reaction, Nitric Oxide Synthase Type I

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