Research Paper Volume 12, Issue 11 pp 10912—10930

Dynamic changes of autophagic flux induced by Abeta in the brain of postmortem Alzheimer’s disease patients, animal models and cell models

Figure 2. The accumulation of APs in the brain tissue of APP/PS1 DTg AD mice. (A) TEM showing little autophagy in wild-type (Wt) mice in the same litter (a-c); APs were also not easily observed in the brains of 3-month-old DTg mice (d); APs could be observed in the brains of 6-month-old DTg mice (e); a large number of APs and ALs had accumulated in the damaged axonal of brain in 10-month-old DTg mice (f). AL: autolysosome, AP: autophagosome, GA: Golgi apparatus, LYS: lysosome, MIT: mitochondria, Scale bar = 500 nm. (B) anti-Aβ 4G8 immunofluorescence staining showing no SPs in the cortex of the wild-type mice (a-c), while many SPs formed by the excessive accumulation of Aβ outside the cells in the cortex of DTg mice, (d-f, The arrow represents SP). Scale bar = 100 μm. (C) Double immunofluorescence staining showing that compared with that in Wt mice (a-d1), the expression of LC3 in 10-month-old APP/PS1 DTg mice increased significantly (e), the expression of CTSB decreased significantly (f), cell nuclei were counterstained with DAPI (g), and the co-expression of autophagosomal and lysosomal markers reduced (h). Scale bar = 20 μm, d1, h1 is a partial magnification of d and h.