This is a well-accepted model for many aspects of human disease; pro-inflammatory cytokines are abundant; mice develop CNS lactic acidosis, increased blood-brain barrier permeability, paralysis, seizures and death; and there are similarities in brain histopathology [17].
Factor H deficient (fH -/-) mice develop spontaneous glomerulonephritis characterized by abundant glomerular C3 fragments.
Eight weeks after birth, TBA2 mice develop neurological impairments together with abundant loss of Purkinje cells (Wirths et al. 2009).
Homozygous P301S Tau mice develop severe tau-pathology with abundant filaments of hyperphosphorylated tau in the cerebral cortex already at young ages [ 14, 21].
C57BL/6J mice injected with α-synuclein fibrils developed abundant Lewy body/Lewy neurite-like pathology, whereas mice injected with soluble α-synuclein did not.
Supplementary Figure 6 Pik3cdE1020K/+ mice develop IgM autoantibodies.
Aged Pten-ΔTreg mice develop non-malignant TH1 inflammation.
Both NOS1-/ and NOS3-/ mice develop age-related hypertrophy, although only NOS3-/ mice are hypertensive.
Eight weeks after birth TBA2 mice developed massive neurological impairments together with abundant loss of Purkinje cells.
The mice developed F.F.I.
