Fig. 3
From: Aβ accumulation causes MVB enlargement and is modelled by dominant negative VPS4A
Aβ42 increases high molecular weight complexes of CHMP2B and ESCRT proteins accumulate in amyloid plaques. a Immunolabelling of APP/PS1 transgenic primary neurons shows Aβ42 colocalizing with CHMP2B-positive vesicles. Scale bar 10 μm, n = 3. b A trend for increased high molecular weight complexes of CHMP2B, a 24 kDa ESCRT-III component, in APP/PS1 transgenic compared to wt neurons is seen on native gel. Treatment with 0.5 μM of Aβ1-42 for 3 h further increases these high molecular weight complexes. However only APP/PS1 transgenic neurons treated with Aβ1-42 show a statistically significant increase in high molecular weight complexes compared to wt. Equal amounts of total protein were loaded into the wells, n = 6; *p < 0.05. c VPS4 colocalizes with Aβ42 in amyloid plaques of 19-month-old APP/PS1 mice. Scale bar 40 μm, n = 4. d Tsg101 colocalizes with both Aβ42 and the neuronal-specific endo-lysosomal marker clavesin 1 and 2 in amyloid plaques of 19-month-old APP/PS1 mice. Scale bar 40 μm, n = 3. e In early plaques present in the 3-month-old Tg19959 mice Tsg101 also colocalized with Aβ42. Scale bar 40 μm, n = 3