Figure 1 | Laboratory Investigation

Figure 1

From: Aged vervet monkeys developing transthyretin amyloidosis with the human disease-causing Ile122 allele: a valid pathological model of the human disease

Figure 1

Histopathological features of aged vervet monkeys. TTR amyloid deposits in the heart (a–c), duodenum (d), subcutaneous fat (e), and kidney (g, h) of an aged vervet monkey. (a, g) Congo red staining under polarized light; (b, d, e, h) immunohistochemical staining using anti-TTR antibody; and (c) electron micrograph of amyloid fibrils in the cardiac specimen. Arrowheads: amyloid deposits in the vascular wall; arrows: absence of amyloid deposits in the kidney glomerulus. (f) Silver stain (lane 1) and immunoblotting using anti-TTR antibody (lane 2) of amyloid proteins extracted from cardiac amyloid deposits. Aged monkeys also developed amyloid β (Aβ) amyloid deposits in the brain (i; immunohistochemical staining using anti-Aβ antibody) and IAPP amyloid deposits in the pancreas (j; immunohistochemical staining using anti-IAPP antibody). is, islet IAPP amyloid deposit; p, Aβ amyloid deposits in senile plaques; v, vascular Aβ amyloid deposits.

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