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Figure 1 | Molecular Neurodegeneration

Figure 1

From: Histopathological and molecular heterogeneity among individuals with dementia associated with Presenilin mutations

Figure 1

Histology and immunocytochemistry of amyloid deposits in PSEN mutations. A) PSEN2 N141I mutation primitive plaques immunoreacted with 10D5 antibody. B) Cotton wool plaques in the PSEN1 A431E mutation immunoreacted with the 21F12. On the upper-right corner there is a mature plaque. C) Cotton wool plaques associated with the PSEN1 A260V mutation immunoreacted with the 10D5 antibody. D) Mature neuritic plaque observed in the PSEN1 A79V mutation. 10D5 antibody. E) Primitive plaque localized the cerebral cortex of the PSEN1 A79V mutation immunoreacted with the 10D5 antibody. F) Cortical amyloid plaques immunoreacted with the 10D5 antibodies at low magnification in the PSEN1 V261F mutation. Numerous CWP and occasional mature core neuritic plaques are observed in addition to severe amyloid angiopathy. G) Cotton wool plaques in the PSEN1 V261F mutation developed with the 10D5 antibody. H) Abundant CWP observed in the PSEN1 V261F stained by hematoxilin and eosin. The plaques are surrounded by a discreet number of reactive astrocytes. In the remaining areas of the field several regions of severe neuronal loss and glyosis and moderate microvacuolization are observed. I) Severe Aβ immunoreactive cerebral amyloid angiopathy in the cerebral cortex of PSEN1 A431E mutation. J) A hematoxylin and eosin stained section of the cerebral cortex of PS1 431E mutation. Magnifications: 63 × (A, B, C, D, E, G); 40 × (I and J); 20 × (H) and 10 × (F). Scale Bars = 20 μm.

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