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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: Co-occurrence of chronic traumatic encephalopathy and prion disease

Fig. 1

Prion histopathology in CTE Cases 1–3. Hematoxylin and eosin (HE) (a, b, f, g, j, k) and PrP immunohistochemistry (c-e, h, i, l, m). a: Severe spongiform degeneration (SD); dashed inset: higher magnification of a core amyloid β (Aβ) plaque; dotted inset: SD with large vacuoles. b: Focal distribution of large vacuoles SD in the molecular layer of the cerebellum; inset: large vacuoles typically affecting the deeper region of the molecular layer. c and d: Widespread “synaptic” PrP immunostaining (c) along with focal coarse and perivacuolar patterns (d); c, inset: enhancement of PrP immunoreactivity around an Aβ plaque. e: Larger and clustered PrP granules co-distributed with small vacuoles SD in the molecular layer; inset: higher magnification in the depth of a sulcus. f: Severe atrophy with gliosis and neuronal loss; arrow: reactive astrocyte. g: Atrophy, gliosis and kuru plaques in the granular cell layer; arrow: reactive astrocyte; arrowhead: kuru plaque. h: Plaques and plaque-like PrP deposits in a background of coarse PrP granules; inset: PrP staining of a kuru plaque. i: Coarse, plaque and plaque-like PrP immunostaining patterns in molecular and granular layers, and deep white matter; inset: cluster of kuru plaques in the granular layer. j: Small vacuoles SD. k: small vacuoles SD; inset: higher magnification. l: “Synaptic” PrP immunostaining. m: Widespread PrP immunostaining with “brush stroke” pattern of PrP deposition (arrow) in molecular layer typical of sCJDMM1; Ab: 3F4. Scale bar in insets: 25 μm (a and c), 20 μm (h) and 50 μm (b, e, i, k)

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