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. 2019 May 10;6(1):17–58. doi: 10.5194/pb-6-17-2019

Figure 2.

Figure 2

Clinical and pathological aspects of marmoset EAE induced with MS myelin/CFA.(a) The graphs show the protracted clinical course, which is variable among individual animals. Case EH has relapsing–remitting disease that could be followed for almost 1 year. The other four cases transit to progressive disease, which can worsen quickly (EK, EL) or more slowly (EI, EJ). (b)  Case EI was subjected to in vivo magnetic resonance imaging (MRI) just before sacrifice. The middle and bottom rows show two horizontal brain slices from a T2-weighted image (middle) and a postcontrast (triple dose Gadolinium-DTPA; bottom) with the position of corresponding lesions indicated. After the scans were made, the monkey was humanely killed, the brain was removed and fixated in toto. Then a new postmortem T2-weighted scan was made. This allowed us to determine the exact position of all lesions that were detected in vivo. (c) The top row shows two coronal sections of the same MRI scan with lesions indicated. The middle and bottom rows show a magnification of individual lesions, which allowed us to conclude that brain lesions in this model are presented in different stages. (d) The top image shows an MRP14 staining of macrophages from lesions I and J, illustrating their inflammatory active nature. Notice that lesion I is one of the two gadolinium contrast-enhancing lesions. The three images below show the histological aspect of lesion J, which is characterized by primary demyelination (LFB staining), sparing of axons (Bielschowsky silver impregnation) and inflammation (MRP14). The macrophage staining shows the heterogeneity of this lesion, which is suggestive of confluent lesions of different age.