Table 2. RML and GPI^-RML prions differ in the oligomerization state and show profound differences in the disease phenotype.

Property	RML in WT mice	GPI-RML in GPI-anchorless PrP expressing mice
Organ tropism	Lymphoid tissue, CNS	Lymphoid tissue, CNS, adipose tissue, skeletal muscle, heart, colon (lamina propria), pancreas (islets of Langerhans), kidney
Neuroinvasion of brain by IO, IP, IV routes	Efficient	Poor, with 25–73% attack rate
Neuroinvasion of brain by IN or IT routes	Efficient	Poor, no prions in brain
PrPSc aggregate morphology in brain	Diffuse PrPSc surrounding astrocytes and/or neurons and in neuropil	Dense fibrillar angiocentric plaques
PrPSc distribution in brain	No vascular PrPSc; diffuse PrPSc deposits particularly in the hippocampus, thalamus, cerebral cortex, cerebral peduncles and septum	Surrounding capillaries and widely distributed throughout the brain
PK resistance	Low	Higher than GPI-anchored state
Conformational stability	0.98+/−0.02	3.21+/−0.09 (3rd psg)

IC: intracerebral; IP: intraperitoneal; IN: intranerval; IT: intratongue; IV: intravenous; IO: intraocular.

Data included are from this study and references28,32,53,54,68,69,70,71,72,73.