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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Duration and selectivity of blood-brain barrier breakdown in chronic relapsing experimental allergic encephalomyelitis studied by gadolinium-DTPA and protein markers.

Gadolinium-DTPA (Gd-DTPA) enhancement seen with magnetic resonance imaging in chronic relapsing experimental allergic encephalomyelitis (CREAE) corresponded with sites of blood-brain barrier breakdown judged by traditional markers in areas of inflammatory demyelination. Duration of Gd-DTPA leakage for individual lesions in CREAE varied from 5 days to more than 5 wks. By contrast, in acute EAE leakage was of shorter duration (always less than 5 days). Selective enhancement was observed in CREAE lesions using Gd-protein markers. Gd-albumin enhancement was not always seen in areas of leakage of the smaller molecular weight compound Gd-DTPA. The addition of immunoglobulin to the gadolinium complex led to enhancement of lesions not seen with Gd-albumin alone. From the similarities between the histology and the patterns of Gd-enhancement in CREAE and multiple sclerosis, it is probable that Gd-enhancement reflects active inflammation (with or without demyelination) in the human disease.[1]

References

  1. Duration and selectivity of blood-brain barrier breakdown in chronic relapsing experimental allergic encephalomyelitis studied by gadolinium-DTPA and protein markers. Hawkins, C.P., Munro, P.M., MacKenzie, F., Kesselring, J., Tofts, P.S., du Boulay, E.P., Landon, D.N., McDonald, W.I. Brain (1990) [Pubmed]
 
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