Lack of secondary pathology in the thalamus after focal cerebral ischemia in nonhuman primates

Remote regions such as the thalamus undergo secondary degeneration after cerebral ischemia. In rodents, the pathology in the thalamus is characterized by a robust inflammatory reaction, β-amyloid (Aβ) accumulation and calcification. Here we studied whether nonhuman primates subjected to middle cerebral artery occlusion (MCAO) display a similar pathology. Common marmosets (n = 4) were subjected to transient MCAO for 3 h. Two sham-operated animals served as controls. All animals underwent MRI examination (T2) on postoperative day 7 to assess the location of the infarct. After a 45-day follow-up period, the animals were perfused for histology to evaluate β-amyloid and calcium load in the peri-infarct regions and the thalamus. There was no Aβ or calcium staining in the sham-operated marmosets. The contralateral hemisphere was devoid of Aβ and calcium staining in MCAO animals, except calcium staining in one animal. In the ipsilateral cortex, patchy groups of Aβ-positive cells were observed. Occasional calcium staining was observed in the peri-infarct regions, lesion core, and remote regions such as the substantia nigra. The most important, the thalamus was devoid of any sign of Aβ and calcium aggregation in MCAO animals. Staining for glial fibrillary acidic protein (GFAP) showed marked astrogliosis in the ipsilateral cortex and thalamus. In conclusion, our preliminary study in marmosets did not identify Aβ and calcium pathology in the thalamus following cerebral ischemia as shown in rodents.