Mitochondrial defects in acute multiple sclerosis lesions
| Autor: | Don J. Mahad, Douglas M. Turnbull, Iryna Ziabreva, Hans Lassmann |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2008 |
| Předmět: |
Male
Pathology Mitochondrial Diseases Respiratory chain multiple sclerosis Pathogenesis PERSISTENT INHIBITION Myelin 0302 clinical medicine cytochrome c oxidase CULTURED HUMAN-CELLS Aged 80 and over 0303 health sciences Mitochondrial respiratory chain complex IV Middle Aged ENCODED SUBUNITS Mitochondria mitochondria Oligodendroglia Mitochondrial respiratory chain medicine.anatomical_structure Acute Disease MYELIN-ASSOCIATED GLYCOPROTEIN Female RESPIRATORY-CHAIN WHITE-MATTER Adult medicine.medical_specialty CYTOCHROME-C-OXIDASE Multiple Sclerosis Pattern III lesion Biology COMPLEX-I White matter Electron Transport Electron Transport Complex IV Mitochondrial Proteins 03 medical and health sciences Mitochondrial Encephalomyopathies medicine Humans 030304 developmental biology Aged NITRIC-OXIDE Multiple sclerosis Diffuse Cerebral Sclerosis of Schilder Original Articles medicine.disease Axons Astrocytes Immunology Neurology (clinical) NEURODEGENERATIVE DISEASES 030217 neurology & neurosurgery |
| Zdroj: | Brain Mahad, D, Ziabreva, I, Lassmann, H & Turnbull, D 2008, ' Mitochondrial defects in acute multiple sclerosis lesions ', Brain, vol. 131, no. 7, pp. 1722-1735 . https://doi.org/10.1093/brain/awn105 |
| ISSN: | 1460-2156 0006-8950 |
| DOI: | 10.1093/brain/awn105 |
| Popis: | Multiple sclerosis is a chronic inflammatory disease, which leads to focal plaques of demyelination and tissue injury in the CNS. The structural and immunopathological patterns of demyelination suggest that different immune mechanisms may be involved in tissue damage. In a subtype of lesions, which are mainly found in patients with acute fulminant multiple sclerosis with Balos type concentric sclerosis and in a subset of early relapsing remitting multiple sclerosis, the initial myelin changes closely resemble those seen in white matter stroke (WMS), suggesting a hypoxia-like tissue injury. Since mitochondrial injury may be involved in the pathogenesis of such lesions, we analysed a number of mitochondrial respiratory chain proteins in active lesions from acute multiple sclerosis and from WMS using immunohistochemistry. Functionally important defects of mitochondrial respiratory chain complex IV [cytochrome c oxidase (COX)] including its catalytic component (COX-I) are present in Pattern III but not in Pattern II multiple sclerosis lesions. The lack of immunohistochemically detected COX-I is apparent in oligodendrocytes, hypertrophied astrocytes and axons, but not in microglia. The profile of immunohistochemically detected mitochondrial respiratory chain complex subunits differs between multiple sclerosis and WMS. The findings suggest that hypoxia-like tissue injury in Pattern III multiple sclerosis lesions may be due to mitochondrial impairment. |
| Databáze: | OpenAIRE |
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