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.