Figure 4.

Effect of sialoadhesin-deficiency on the neuropathology in the brains of prion-infected mice. (a) Sialoadhesin-deficiency had no observable effect on disease-specific vacuolation, PrP^d deposition, or reactive glial responses in the brains of the clinically affected, peripheral prion-infected mice. High levels of spongiform pathology (haematoxylin & eosin, top row), heavy accumulations of disease-specific prion protein (PrP) (brown, second row), reactive astrocytes expressing glial fibrillary acidic protein (GFAP) (brown, third row), and active microglia expressing Iba1 (brown, bottom row) were detected in the brains of all clinically prion disease-affected wild-type (WT) mice (left-hand column) and sialoadhesin-deficient (Sn^−/−) mice (right-hand column). (b) Pathological assessment of the spongiform change (vacuolation) in brains from terminally prion-affected WT (blue line) and Sn^−/− (red line) mice. Vacuolation was scored on a scale of 0–5 in the following grey (G1–G9) and white (W1–W3) matter areas: G1, dorsal medulla; G2, cerebellar cortex; G3, superior colliculus; G4, hypothalamus; G5, thalamus; G6, hippocampus; G7, septum; G8, retrosplenial and adjacent motor cortex; G9, cingulate and adjacent motor cortex; W1, inferior and middle cerebellar peduncles; W2, decussation of superior cerebellar peduncles; and W3, cerebellar peduncles.