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Pain in the brain

View Article: PubMed Central

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On page 2473, Hinson and colleagues demonstrate how the disease's distinguishing autoantibody disrupts glutamate regulation... Neuromyelitis optica (NMO), also known as Devic's disease, results in MS-like lesions in the optic nerves and along the spine... Yet unlike MS, NMO is associated with production of a specific autoantibody known as NMO-IgG... In 2005, the same group identified NMO-IgG's target as aquaporin-4, a water channel protein concentrated in astrocyte membranes along the blood-brain barrier... However, the finding was somewhat perplexing because myelin damage occurs on nerve cells, not on astrocytes... Now the team confirms that astrocytes are indeed the relevant target, and show how autoantibody binding can lead to demyelination... When NMO-IgG binds to aquaporin-4, they show, the levels of the astrocyte glutamate transporter EAAT2 drop... After spelling out the pathway in astrocyte in vitro assays, the team examined human tissue... Sure enough, NMO lesions along cadaver spines lacked both aquaporin-4 and EAAT2... Lesions from MS patients show no such deficiencies, highlighting another way in which the demyelinating disorders differ... If the groups' results are confirmed in vivo, drug development could be straightforward.

No MeSH data available.


Aquaporin-4 (red) and EAAT2 (green) colocalize in normal spine.
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fig1: Aquaporin-4 (red) and EAAT2 (green) colocalize in normal spine.


Pain in the brain
Aquaporin-4 (red) and EAAT2 (green) colocalize in normal spine.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2571916&req=5

fig1: Aquaporin-4 (red) and EAAT2 (green) colocalize in normal spine.

View Article: PubMed Central

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

On page 2473, Hinson and colleagues demonstrate how the disease's distinguishing autoantibody disrupts glutamate regulation... Neuromyelitis optica (NMO), also known as Devic's disease, results in MS-like lesions in the optic nerves and along the spine... Yet unlike MS, NMO is associated with production of a specific autoantibody known as NMO-IgG... In 2005, the same group identified NMO-IgG's target as aquaporin-4, a water channel protein concentrated in astrocyte membranes along the blood-brain barrier... However, the finding was somewhat perplexing because myelin damage occurs on nerve cells, not on astrocytes... Now the team confirms that astrocytes are indeed the relevant target, and show how autoantibody binding can lead to demyelination... When NMO-IgG binds to aquaporin-4, they show, the levels of the astrocyte glutamate transporter EAAT2 drop... After spelling out the pathway in astrocyte in vitro assays, the team examined human tissue... Sure enough, NMO lesions along cadaver spines lacked both aquaporin-4 and EAAT2... Lesions from MS patients show no such deficiencies, highlighting another way in which the demyelinating disorders differ... If the groups' results are confirmed in vivo, drug development could be straightforward.

No MeSH data available.