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. 2013 Jul 25;1:40. doi: 10.1186/2051-5960-1-40

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Copyright © 2013 Popescu et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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AQP1, AQP4 and GFAP protein expression in human CPM lesions. (a-d) A demyelinated lesion in the central basis pontis(a) of a 56-year-old man with CPM in context of rapidly corrected hyponatremia shows loss of astrocytic AQP4 extending beyond the area of demyelination (b), loss of AQP1 (c), but retained GFAP (d); (e-h) A CPM lesion in the central basis pontis of a 53-year-old man with CPM and severe dehydration, malnutrition and hypernatremia shows relative preservation of myelin (e), loss of astrocytic AQP4 (f), AQP1 (g), but preserved GFAP (h); (i-l) A demyelinated lesion in the central basis pontis(i) of a 24-year-old woman with CPM in the context of hepatic failure and hypokalemia shows increased AQP4 (j), AQP1 (k) and GFAP expression (l); (a, e, i) PLP; (b,f, j) AQP4; (c, g, k) AQP1; (d, h, l) GFAP; (scale bar = 5 mm).

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