Neuroinvasion in Prion Diseases: The Roles of Ascending Neural Infection and Blood Dissemination
Figure 6
CVO involvement may contribute to the spread of infection into the brain parenchyma. Preclinically affected TSE sheep show mild early PrPd accumulation in the median eminence (ME) (a; x4), or severe deposition in later stages (b; x4). Higher magnification is needed to detect mild PrPd accumulation in the ME (c; x60). In later stages, preclinical sheep do show accumulation of PrPd in those brain areas with established connections with the CVOs. A sagittal section of the diencephalon (d; x1) has been produced from the area compressed in the white rectangle in the macroscopic sagittal view of the brain highlighting some of the neural structures. Thus, the involvement of the ME correlates with PrPd accumulation in the arcuate nucleus (ARQ) (a,b,e), and that of the organum vasculosum of the lamina terminalis (OVLT) and the subfornical organ (SFO) correlates with PrPd in several nuclei: preoptic (PON) (f, x1), suprachiasmatic (SQN) (g; x4), supraoptic (SOP) (e, x1), paraventricular (PVN) (d, e), bed nucleus of the stria terminalis (BNST) (d) and perifornical (PFN) (f). Such correlations are difficult in the vagal complex because of the widespread severe PrPd accumulation (h).
