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Genetic dissection of neurodegeneration and CNS inflammation

Olsson, Tomas; Piehl, Fredrik; Swanberg, Maria LU and Lidman, Olle (2005) In Journal of the Neurological Sciences 233(1-2). p.99-108
Abstract

Inflammation and neurodegeneration characterize multiple sclerosis, as well as many other diseases of the central nervous system (CNS). The understanding of the molecular pathways that regulate these processes is of fundamental importance for the development of new therapies. Nerve lesions paradigms in animals can serve as important tools to dissect central features of human CNS disease and by using these models certain key regulators have also been identified. However, our knowledge of how aspects of neurodegeneration and CNS inflammation are regulated on a genomic level is very limited. Such knowledge may help to unravel disease mechanisms. By using a standardized nerve trauma model, ventral root avulsion (VRA), in a series of inbred... (More)

Inflammation and neurodegeneration characterize multiple sclerosis, as well as many other diseases of the central nervous system (CNS). The understanding of the molecular pathways that regulate these processes is of fundamental importance for the development of new therapies. Nerve lesions paradigms in animals can serve as important tools to dissect central features of human CNS disease and by using these models certain key regulators have also been identified. However, our knowledge of how aspects of neurodegeneration and CNS inflammation are regulated on a genomic level is very limited. Such knowledge may help to unravel disease mechanisms. By using a standardized nerve trauma model, ventral root avulsion (VRA), in a series of inbred rat strains we here demonstrate a potent genetic regulation of the degree of neuron death and glial activation. Genome wide mapping of these phenotypes in experimental rat strain crosses identifies several quantitative trait loci (QTLs) controlling nerve lesion-induced nerve cell death, local T cell accumulation and expression of MHC class II on microglia. This approach may lead to the identification of evolutionary conserved genetic polymorphisms in key controlling genes, which can serve as prime candidates for association studies in several human CNS diseases.

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author
publishing date
type
Contribution to journal
publication status
published
keywords
Animals, Central Nervous System Diseases, Chromosome Mapping, Crosses, Genetic, Disease Models, Animal, Humans, Inflammation, Models, Biological, Neurodegenerative Diseases, Neuroglia, Journal Article, Review
in
Journal of the Neurological Sciences
volume
233
issue
1-2
pages
10 pages
publisher
Elsevier
external identifiers
  • scopus:20444391696
ISSN
0022-510X
DOI
10.1016/j.jns.2005.03.020
language
English
LU publication?
no
id
f11cfeff-cf56-4ba0-a12d-07134f4c8e04
date added to LUP
2017-02-22 09:53:13
date last changed
2017-02-26 04:46:06
@article{f11cfeff-cf56-4ba0-a12d-07134f4c8e04,
  abstract     = {<p>Inflammation and neurodegeneration characterize multiple sclerosis, as well as many other diseases of the central nervous system (CNS). The understanding of the molecular pathways that regulate these processes is of fundamental importance for the development of new therapies. Nerve lesions paradigms in animals can serve as important tools to dissect central features of human CNS disease and by using these models certain key regulators have also been identified. However, our knowledge of how aspects of neurodegeneration and CNS inflammation are regulated on a genomic level is very limited. Such knowledge may help to unravel disease mechanisms. By using a standardized nerve trauma model, ventral root avulsion (VRA), in a series of inbred rat strains we here demonstrate a potent genetic regulation of the degree of neuron death and glial activation. Genome wide mapping of these phenotypes in experimental rat strain crosses identifies several quantitative trait loci (QTLs) controlling nerve lesion-induced nerve cell death, local T cell accumulation and expression of MHC class II on microglia. This approach may lead to the identification of evolutionary conserved genetic polymorphisms in key controlling genes, which can serve as prime candidates for association studies in several human CNS diseases.</p>},
  author       = {Olsson, Tomas and Piehl, Fredrik and Swanberg, Maria and Lidman, Olle},
  issn         = {0022-510X},
  keyword      = {Animals,Central Nervous System Diseases,Chromosome Mapping,Crosses, Genetic,Disease Models, Animal,Humans,Inflammation,Models, Biological,Neurodegenerative Diseases,Neuroglia,Journal Article,Review},
  language     = {eng},
  number       = {1-2},
  pages        = {99--108},
  publisher    = {Elsevier},
  series       = {Journal of the Neurological Sciences},
  title        = {Genetic dissection of neurodegeneration and CNS inflammation},
  url          = {http://dx.doi.org/10.1016/j.jns.2005.03.020},
  volume       = {233},
  year         = {2005},
}