The DOI matches its Crossref record; 70 of the 70 references it cites were found in a registry or an index.
BDNF and gp145trkB in multiple sclerosis brain lesions: neuroprotective interactions between immune and neuronal cells?
Open accessAbstract
Recent immunohistological and imaging studies emphasize the crucial role of axonal injury in determining the extent of permanent neurological deficits in patients with multiple sclerosis. We have recently shown that human immune cells are capable of producing the neurotrophin brain-derived neurotrophic factor (BDNF), which can prevent axonal and neuronal damage after various pathological insults. BDNF imported into the CNS by immune cells would thus be an attractive candidate for mediating neuroprotective effects in multiple sclerosis. The aim of the present study was to perform a detailed immunohistochemical analysis of the expression of BDNF and its receptor truncated trkB tyrosine kinase receptor (gp145trkB) in a series of multiple sclerosis brain lesions. Our data show that various types of neurones throughout the brain are BDNF immunopositive in multiple sclerosis patients as well as in controls. Furthermore, in multiple sclerosis lesions, BDNF is primarily present in immune cells (T cells, macrophages/microglia) and reactive astrocytes. The number of BDNF immunopositive cells correlates with lesional demyelinating activity. The BDNF receptor gp145trkB is found in neurones in the immediate vicinity of multiple sclerosis plaques as well as in reactive astrocytes within the lesion, but not in immune cells. Our results demonstrate that both BDNF and gp145trkB are expressed in multiple sclerosis lesions. This suggests that BDNF and gp145trkB are involved in immune-mediated neuroprotective interactions in multiple sclerosis, and supports the concept that immune cells produce both damaging and protective factors in multiple sclerosis lesions.
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Cites
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“…into sites of neural injury seem to protect brainstem neurones after experimental trauma (Serpe et al., 1999) and could potentially do so in neurodegenerative diseases (Batchelor et al., 1999), which show substantial immune activation in foci of pathological change (McGeer and McGeer, 1995).”
BackgroundKerschensteiner, M., Gallmeier, E., Behrens, L., Leal, V. V., Misgeld, T., Klinkert, W. E. F., Kolbeck, R., Hoppe, E., Oropeza-Wekerle, R.-L., Bartke, I., et al. (1999) · The Journal of Experimental Medicine · doi:10.1084/jem.189.5.865 · Cited by 1,019
Self-citationRegional distribution of brain-derived neurotrophic factor mRNA in the adult mouse brain.
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Acute axonal injury in multiple sclerosis: Correlation with demyelination and inflammation
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Cited by
Microglia: Active sensor and versatile effector cells in the normal and pathologic brain
Hanisch, U.-K., & Kettenmann, H. (2007) · Nature Neuroscience · doi:10.1038/nn1997 · Cited by 3,676
Microglial physiology: unique stimuli, specialized responses
Ransohoff, R. M., & Perry, V. H. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132528 · Cited by 1,858
The therapeutic potential of neural stem cells
Martino, G., & Pluchino, S. (2006) · Nature Reviews Neuroscience · doi:10.1038/nrn1908 · Cited by 744
Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis
Friese, M. A., Schattling, B., & Fugger, L. (2014) · Nature Reviews Neurology · doi:10.1038/nrneurol.2014.37 · Cited by 628
Coles, A. J., Cox, A., Page, E., Jones, J., Trip, S. A., Deans, J., Seaman, S., Miller, D. H., Hale, G., Waldmann, H., et al. (2006) · Journal of Neurology · doi:10.1007/s00415-005-0934-5 · Cited by 506
Metadata
- Authors
- Stadelmann, C., Kerschensteiner, M., Misgeld, T., Brück, W., Hohlfeld, R., & Lassmann, H.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-01-01
- Volume
- 125
- Issue
- 1
- Pages
- 75-85
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2133005541
- Cited by
- 425
- References
- 70
- FWCI
- 17.28
- Type
- journal article
- Language
- en
- Open access
- bronze
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