Experimental autoimmune encephalomyelitis (EAE) IN C57Bl/6 mice is not associated with astrogliosis

Pham, Hong; Doerrbecker, Juliane; Ramp, Anton A.; D'Souza, Claretta S; Gorasia, Dhana G.; Purcell, Anthony W.; Ayers, Margaret; Orian, Jacqueline M.

doi:10.1016/j.jneuroim.2010.10.006

Cited by 23 publications

(30 citation statements)

References 58 publications

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“…However, the use of the C57Bl/6 variant is complicated by the occurrence of multiple clinical profiles (chronic, multiphasic or monophasic) and unpredictability of disease course within a given cohort (Berard et al 2010;Bernard et al 1998). Additionally, we have shown that the pathology in this variant is associated with a progressively diminishing astrogliosis with increasing clinical score, a feature which is not associated with MS pathology (Ayers et al 2004;Onuki et al 2001;Pham et al 2009Pham et al , 2011Wang et al 2005). The use of transgenic and gene deletion mutants in the NOD/Lt background in a number of investigations (Anderson et al 2012;Cannon et al 2008;Mars et al 2002Mars et al , 2008McQualter et al 2001) suggests that generation of such genetically modified strains does not present any particular technical difficulty.…”

Section: Future Studiesmentioning

confidence: 80%

“…The antigen is delivered in two s.c. injections in the inguinal region and is followed by two i.v. injections of PTx at days 0 and 2, of 350 ng each (Wang et al 2005;Pham et al 2009Pham et al , 2011. Vehicle-only control mice receive the same treatment, but with the omission of MOG peptide.…”

Section: Clinical Profile and Lesion Topography In Mog 35-55 -Inducedmentioning

confidence: 99%

“…The timing of subsequent attacks is less predictable. Mice experience between 1 and 3 additional attacks between 25 and 30, 35 and 40 and 43 and 50 dpi, before reaching the progressive stage by about day 60 (Pham et al 2011;Wang et al 2005). For a detailed histopathological evaluation of lesion topography during the first attack, a procedure is fully described in Orian et al 2014.…”

Section: Clinical Profile and Lesion Topography In Mog 35-55 -Inducedmentioning

confidence: 99%

See 2 more Smart Citations

Modelling MS: Chronic-Relapsing EAE in the NOD/Lt Mouse Strain

Dang

Bui

D'Souza

et al. 2015

Current Topics in Behavioral Neurosciences

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Modelling complex disorders presents considerable challenges, and multiple sclerosis (MS) is no exception to this rule. The aetiology of MS is unknown, and its pathophysiology is poorly understood. Moreover, the last two decades have witnessed a dramatic revision of the long-held view of MS as an inflammatory demyelinating white matter disease. Instead, it is now regarded as a global central nervous system (CNS) disorder with a neurodegenerative component. Currently, there is no animal model recapitulating MS immunopathogenesis. Available models are based on autoimmune-mediated demyelination, denoted experimental autoimmune encephalomyelitis (EAE) or virally or chemically induced demyelination. Of these, the EAE model has been the most commonly used. It has been extensively improved since its first description and now exists as a number of variants, including genetically modified and humanized versions. Nonetheless, EAE is a distinct disease, and each variant models only certain facets of MS. Whilst the search for more refined MS models must continue, it is important to further explore where mechanisms underlying EAE provide proof-of-principle for those driving MS pathogenesis. EAE variants generated with the myelin component myelin oligodendrocyte glycoprotein (MOG) have emerged as the preferred ones, because in this particular variant disease is associated with both T- and B-cell effector mechanisms, together with demyelination. MOG-induced EAE in the non-obese diabetic (NOD) mouse strain exhibits a chronic-relapsing EAE clinical profile and high disease incidence. We describe the generation of this variant, its contribution to the understanding of MS immune and pathogenetic mechanisms and potential for evaluation of candidate therapies.

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Section: Future Studiesmentioning

confidence: 80%

Section: Clinical Profile and Lesion Topography In Mog 35-55 -Inducedmentioning

confidence: 99%

Section: Clinical Profile and Lesion Topography In Mog 35-55 -Inducedmentioning

confidence: 99%

See 1 more Smart Citation

Modelling MS: Chronic-Relapsing EAE in the NOD/Lt Mouse Strain

Dang

Bui

D'Souza

et al. 2015

Current Topics in Behavioral Neurosciences

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Section: Future Studiesmentioning

confidence: 81%

Emerging and Evolving Topics in Multiple Sclerosis Pathogenesis and Treatments

Flamme¹,

Orian²

2015

Current Topics in Behavioral Neurosciences

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Current Topics in Behavioral Neurosciences provides critical and comprehensive discussions of the most significant areas of behavioral neuroscience research, written by leading international authorities. Each volume offers an informative and contemporary account of its subject, making it an unrivalled reference source. Titles in this series are available in both print and electronic formats.With the development of new methodologies for brain imaging, genetic and genomic analyses, molecular engineering of mutant animals, novel routes for drug delivery, and sophisticated cross-species behavioral assessments, it is now possible to study behavior relevant to psychiatric and neurological diseases and disorders on the physiological level. The Behavioral Neurosciences series focuses on ''translational medicine'' and cutting-edge technologies. Preclinical and clinical trials for the development of new diagnostics and therapeutics as well as prevention efforts are covered whenever possible.

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“…Furthermore, because the correlation between neuroinflammation and neurodegenerative disease is so strong-and because neuroinflammation could play an important role in the pathogenesis of neurodegenerative disease such as Alzheimer's disease (AD) [9, 10]-AQP4 may indeed protect against neurodegenerative disease [11]. AQP4 is associated with neuroinflammation in chronic and acute brain diseases [5,[12][13][14][15][16][17][18]. Because AQP4 is mostly expressed in the astrocytes, and because neuroinflammation is characterized by both phenotypic changes of resting astrocytes to astrogliosis and microglial activation, investigating this question may lead to a better understanding of many brain diseases.…”

Section: Introductionmentioning

confidence: 99%

A research update on the potential roles of aquaporin 4 in neuroinflammation

et al. 2015

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The presence of aquaporins (AQPs) in the brain has led to intense research on the underlying roles of this family of proteins under both normal and pathological conditions. Aquaporin 4 (AQP4) is the major water-channel membrane protein expressed in the central nervous system (CNS), primarily in astrocytes. Emerging evidence suggests that AQP4 could play an important role in water and ion homeostasis in the brain, and it has been studied in various brain pathological conditions. However, far less is known about the potential for AQP4 to influence neuroinflammation and, furthermore, its potential role in neurodegenerative disorders such as Alzheimer's disease (AD). It has been suggested that the pathogenesis of many clinical diseases, such as neuromyelitis optica (NMO), multiple sclerosis (MS) and brain injuries, is related to the regulation of AQP4 expression. Investigating the effects of AQP4 on microglia and astrocytes could be important to understand its role in the pathogenesis of neuroinflammation. Although the exact roles of non-steroidal anti-inflammatory drugs (NSAIDs) in protection against the detrimental effects of neuroinflammation remain unclear, research into the possible neuroprotective effects of AQP4 against neuroinflammation regulation seems to be important for future investigations.

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Experimental autoimmune encephalomyelitis (EAE) IN C57Bl/6 mice is not associated with astrogliosis

Cited by 23 publications

References 58 publications

Modelling MS: Chronic-Relapsing EAE in the NOD/Lt Mouse Strain

Modelling MS: Chronic-Relapsing EAE in the NOD/Lt Mouse Strain

Emerging and Evolving Topics in Multiple Sclerosis Pathogenesis and Treatments

A research update on the potential roles of aquaporin 4 in neuroinflammation

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