Skip to main content
Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Astrocytic autophagy plasticity modulates Aβ clearance and cognitive function in Alzheimer’s disease

Fig. 1

Astrocytes induce autophagy components (LC3B and SQSTM1) in response to Aβ oligomer but neurons do not. a, Experimental scheme for detecting autophagy components in primary mouse astrocyte and neuron culture. b, Quantification of GFAP or MAP2 immunoreactivity in the primary mouse astrocyte and neuron coculture system with or without Aβ oligomer. A total of 400 cell count, 50 cells/well, n = 8 wells. c, Double immunostaining with GFAP and LC3B antibodies in the primary culture system. Scale bar (white): 50 μm d, Quantification of LC3B immunoreactivity in GFAP-positive astrocytes and their correlation graphs with GFAP intensity. A total of 200 cell count, 50 cells/well, n = 4 wells. e, Double immunostaining with GFAP and SQSTM1 antibodies in the primary culture system. Scale bars (white): 50 μm. f, Quantification of SQSTM1 immunoreactivity in GFAP-positive astrocytes and their correlation graphs with GFAP intensity. A total of 200 cell count, 50 cells/well, n = 4 wells. g, Double immunostaining with MAP2 and LC3B antibodies in the primary culture system. Scale bar (white): 50 μm. h, Quantification of LC3B immunoreactivity in MAP2-positive regions and their correlation graphs with MAP2 intensity. A total of 200 cell count, 50 cells/well, n = 4 wells. i, Double immunostaining with MAP2 and SQSTM1 antibodies in the culture system. Scale bar: 50 μm. j, Quantification of SQSTM1 immunoreactivity in MAP2-positive regions and their correlation graphs with MAP2 intensity. A total of 200 cell count, 50 cells/well, n = 4 wells. A.U.: arbitrary unit, pixel. Significantly different at **, p < 0.01

Back to article page