PMID- 11834594
OWN - NLM
STAT- MEDLINE
DCOM- 20020301
LR  - 20190513
IS  - 0006-8950 (Print)
IS  - 0006-8950 (Linking)
VI  - 125
IP  - Pt 1
DP  - 2002 Jan
TI  - BDNF and gp145trkB in multiple sclerosis brain lesions: neuroprotective 
      interactions between immune and neuronal cells?
PG  - 75-85
AB  - 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.
FAU - Stadelmann, Christine
AU  - Stadelmann C
AD  - Institute for Neuropathology, Charite, Humboldt-University, Berlin, Germany.
FAU - Kerschensteiner, Martin
AU  - Kerschensteiner M
FAU - Misgeld, Thomas
AU  - Misgeld T
FAU - Bruck, Wolfgang
AU  - Bruck W
FAU - Hohlfeld, Reinhard
AU  - Hohlfeld R
FAU - Lassmann, Hans
AU  - Lassmann H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Brain
JT  - Brain : a journal of neurology
JID - 0372537
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Neuroprotective Agents)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Animals
MH  - Astrocytes/chemistry
MH  - Brain/cytology/immunology/*pathology
MH  - Brain Chemistry
MH  - Brain-Derived Neurotrophic Factor/*analysis
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - Male
MH  - Microglia/*chemistry/immunology
MH  - Middle Aged
MH  - Multiple Sclerosis/immunology/*metabolism/pathology
MH  - Neurons/*chemistry
MH  - Neuroprotective Agents/analysis
MH  - Receptor, trkB/*analysis
MH  - T-Lymphocytes/*chemistry/immunology
EDAT- 2002/02/09 10:00
MHDA- 2002/03/02 10:01
CRDT- 2002/02/09 10:00
PHST- 2002/02/09 10:00 [pubmed]
PHST- 2002/03/02 10:01 [medline]
PHST- 2002/02/09 10:00 [entrez]
AID - 10.1093/brain/awf015 [doi]
PST - ppublish
SO  - Brain. 2002 Jan;125(Pt 1):75-85. doi: 10.1093/brain/awf015.