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Neuromyelitis optica pathogenesis and aquaporin 4

Overview of attention for article published in Journal of Neuroinflammation, May 2008
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Neuromyelitis optica pathogenesis and aquaporin 4
Published in
Journal of Neuroinflammation, May 2008
DOI 10.1186/1742-2094-5-22
Pubmed ID

David J Graber, Michael Levy, Douglas Kerr, William F Wade


Neuromyelitis optica (NMO) is a severe, debilitating human disease that predominantly features immunopathology in the optic nerves and the spinal cord. An IgG1 autoantibody (NMO-IgG) that binds aquaporin 4 (AQP4) has been identified in the sera of a significant number of NMO patients, as well as in patients with two related neurologic conditions, bilateral optic neuritis (ON), and longitudinal extensive transverse myelitis (LETM), that are generally considered to lie within the NMO spectrum of diseases. NMO-IgG is not the only autoantibody found in NMO patient sera, but the correlation of pathology in central nervous system (CNS) with tissues that normally express high levels of AQP4 suggests NMO-IgG might be pathogenic. If this is the case, it is important to identify and understand the mechanism(s) whereby an immune response is induced against AQP4. This review focuses on open questions about the "events" that need to be understood to determine if AQP4 and NMO-IgG are involved in the pathogenesis of NMO. These questions include: 1) How might AQP4-specific T and B cells be primed by either CNS AQP4 or peripheral pools of AQP4? 2) Do the different AQP4-expressing tissues and perhaps the membrane structural organization of AQP4 influence NMO-IgG binding efficacy and thus pathogenesis? 3) Does prior infection, genetic predisposition, or underlying immune dysregulation contribute to a confluence of events which lead to NMO in select individuals? A small animal model of NMO is essential to demonstrate whether AQP4 is indeed the incipient autoantigen capable of inducing NMO-IgG formation and NMO. If the NMO model is consistent with the human disease, it can be used to examine how changes in AQP4 expression and blood-brain barrier (BBB) integrity, both of which can be regulated by CNS inflammation, contribute to inductive events for anti-AQP4-specific immune response. In this review, we identify reagents and experimental questions that need to be developed and addressed to enhance our understanding of the pathogenesis of NMO. Finally, dysregulation of tolerance associated with autoimmune disease appears to have a role in NMO. Animal models would allow manipulation of hormone levels, B cell growth factors, and other elements known to increase the penetrance of autoimmune disease. Thus an AQP4 animal model would provide a means to manipulate events which are now associated with NMO and thus demonstrate what set of events or multiplicity of events can push the anti-AQP4 response to be pathogenic.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 183 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Brazil 3 2%
South Africa 2 1%
France 1 <1%
Germany 1 <1%
United Kingdom 1 <1%
Argentina 1 <1%
Japan 1 <1%
United States 1 <1%
Unknown 172 94%

Demographic breakdown

Readers by professional status Count As %
Researcher 29 16%
Student > Ph. D. Student 27 15%
Student > Master 22 12%
Student > Bachelor 20 11%
Other 20 11%
Other 41 22%
Unknown 24 13%
Readers by discipline Count As %
Medicine and Dentistry 70 38%
Agricultural and Biological Sciences 25 14%
Neuroscience 23 13%
Biochemistry, Genetics and Molecular Biology 8 4%
Immunology and Microbiology 7 4%
Other 10 5%
Unknown 40 22%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 March 2022.
All research outputs
of 23,381,576 outputs
Outputs from Journal of Neuroinflammation
of 2,702 outputs
Outputs of similar age
of 84,274 outputs
Outputs of similar age from Journal of Neuroinflammation
of 6 outputs
Altmetric has tracked 23,381,576 research outputs across all sources so far. This one is in the 44th percentile – i.e., 44% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,702 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.7. This one is in the 49th percentile – i.e., 49% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 84,274 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 18th percentile – i.e., 18% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 6 others from the same source and published within six weeks on either side of this one. This one has scored higher than 4 of them.