Fig. 1
From: Contribution of amyloid deposition from oligodendrocytes in a mouse model of Alzheimer’s disease
BACE1 was abolished inBace1fl/fl;Olig2-Cremice. (A) Representative images of fluorescent in situ hybridization to double-probing Bace1mRNA (white) / Syp mRNA (red, neuronal marker) and Bace1 mRNA (white) / Mbp mRNA (red, oligodendrocyte marker) in the gray matter and white matter of cerebral cortex in 4-month-old Bace1fl/fl and Bace1fl/fl;Olig2-Cre brains (N = 3). Scale bar, 20 μm. (B) Immunoblot analysis of BACE1 and full-length APP in 4-month-old Bace1fl/fl and Bace1fl/fl;Olig2-Cre hippocampi. Antibody to β-actin was used as loading control. Blot measurements are in kilodaltons (kDa). (C) Bar graph shows quantification of relative protein levels based on the blot shown in B. N = 3 independent experiments. (D) Immunoblot analysis of BACE1, full-length APP, CTF-83, and Olig2 as measured in the O4+ cells which were isolated from P13 forebrains in Bace1fl/fl and Bace1fl/fl;Olig2-Cre pups. Antibody to β-actin was used as loading control. Blot measurements are in kilodaltons (kDa). (E) Bar graph shows quantification of relative protein levels based on the blot shown in D. N = 3 independent experiments; five pups were used to isolate O4+ immature and mature oligodendrocytes in each group. ***P < 0.001, two-tailed Student’s t test. Values are expressed as mean ± SD