Histopathological patterns of prion disease and Lin5050 positive plaques in <i>Tg</i>(MoPrP^169F) mice.

<p><b>(A)</b> Brain sections from RML-infected <i>Tg</i>(MoPrP^169F);<i>Prnp</i>^-/-, <i>Tg</i>(MoPrP^169F);<i>Prnp</i>^+/-, <i>Prnp</i>^<i>-/-</i> and <i>Prnp</i>^+/+ mice, as well as <i>Tg</i>a20 and <i>Tg81</i> mice inoculated with <i>Tg</i>(MoPrP^169F);<i>Prnp</i>^-/- brain homogenates. Hallmarks of prion disease including vacuolation (hematoxylin and eosin; HE), astrogliosis (glial fibrillary acidic protein; GFAP) and microglial activation (activated microglial marker; IBA1), were detected in terminally sick <i>Tg</i>(MoPrP^169F) and RML-infected wild-type <i>Prnp</i>^+/+ mice. RML-infected wild-type (wt) mice showed the typical diffuse synaptic pattern of SAF84 positive signals (first row), and <i>Tg</i>(MoPrP^169F);<i>Prnp</i>^+/- showed some plaque-like deposits (asterisk; third row). Few weakly stained PrP^Sc deposits were visible in <i>Tg</i>(MoPrP^169F);<i>Prnp</i>^-/- and no PrP signals in <i>Prnp</i>^-/- brains (rows 2 and 4). After passage of <i>Tg</i>(MoPrP^169F);<i>Prnp</i>^-/- brain homogenate into <i>Tg</i>a20 mice, synaptic and plaque-like PrP deposits were observed in the cortex (5^th row). Passage of 263K-infected <i>Tg</i>(MoPrP^169F);<i>Prnp</i>^-/- into <i>Tg</i>81 mice resulted in a prion disease with PrP plaque formation in the cortex (6^th row). Scale bar: 50 μm. (B) Frozen section (10 μm) of <i>Tg</i>(MoPrP^169F);<i>Prnp</i>^-/- brain showed LIN5050 stained aggregates. Fluorescence emission spectra were recorded in 5 regions (M0-M4) at 500–800 nm and compared to the surrounding tissue (M5-M6) (magnification 100x). (C) Same as (B) but from a <i>Tg</i>(MoPrP^169F);<i>Prnp</i>^+/- mouse (magnification 40x).