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

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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.