PMID- 21371012
OWN - NLM
STAT- MEDLINE
DCOM- 20120325
LR  - 20220408
IS  - 1476-5381 (Electronic)
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 164
IP  - 4
DP  - 2011 Oct
TI  - Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis 
      (MS).
PG  - 1079-106
LID - 10.1111/j.1476-5381.2011.01302.x [doi]
AB  - Experimental autoimmune encephalomyelitis (EAE) is the most commonly used 
      experimental model for the human inflammatory demyelinating disease, multiple 
      sclerosis (MS). EAE is a complex condition in which the interaction between a 
      variety of immunopathological and neuropathological mechanisms leads to an 
      approximation of the key pathological features of MS: inflammation, 
      demyelination, axonal loss and gliosis. The counter-regulatory mechanisms of 
      resolution of inflammation and remyelination also occur in EAE, which, therefore 
      can also serve as a model for these processes. Moreover, EAE is often used as a 
      model of cell-mediated organ-specific autoimmune conditions in general. EAE has a 
      complex neuropharmacology, and many of the drugs that are in current or imminent 
      use in MS have been developed, tested or validated on the basis of EAE studies. 
      There is great heterogeneity in the susceptibility to the induction, the method 
      of induction and the response to various immunological or neuropharmacological 
      interventions, many of which are reviewed here. This makes EAE a very versatile 
      system to use in translational neuro- and immunopharmacology, but the model needs 
      to be tailored to the scientific question being asked. While creating 
      difficulties and underscoring the inherent weaknesses of this model of MS in 
      straightforward translation from EAE to the human disease, this variability also 
      creates an opportunity to explore multiple facets of the immune and neural 
      mechanisms of immune-mediated neuroinflammation and demyelination as well as 
      intrinsic protective mechanisms. This allows the eventual development and 
      preclinical testing of a wide range of potential therapeutic interventions.
CI  - (c) 2011 The Authors. British Journal of Pharmacology (c) 2011 The British 
      Pharmacological Society.
FAU - Constantinescu, Cris S
AU  - Constantinescu CS
AD  - Division of Clinical Neurology, School of Clinical Sciences, University of 
      Nottingham, Queen's Medical Centre, Nottingham, UK. 
      cris.constantinescu@nottingham.ac.uk
FAU - Farooqi, Nasr
AU  - Farooqi N
FAU - O'Brien, Kate
AU  - O'Brien K
FAU - Gran, Bruno
AU  - Gran B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
SB  - IM
MH  - Animals
MH  - *Disease Models, Animal
MH  - Drug Design
MH  - Drug Evaluation, Preclinical
MH  - Encephalomyelitis, Autoimmune, Experimental/chemically induced/drug 
      therapy/*immunology/*pathology
MH  - Female
MH  - Haplorhini
MH  - Humans
MH  - Male
MH  - Mice
MH  - Multiple Sclerosis/diagnosis/*drug therapy/immunology/*pathology
MH  - Rats
PMC - PMC3229753
EDAT- 2011/03/05 06:00
MHDA- 2012/03/27 06:00
PMCR- 2012/10/01
CRDT- 2011/03/05 06:00
PHST- 2011/03/05 06:00 [entrez]
PHST- 2011/03/05 06:00 [pubmed]
PHST- 2012/03/27 06:00 [medline]
PHST- 2012/10/01 00:00 [pmc-release]
AID - 10.1111/j.1476-5381.2011.01302.x [doi]
PST - ppublish
SO  - Br J Pharmacol. 2011 Oct;164(4):1079-106. doi: 10.1111/j.1476-5381.2011.01302.x.