Fig. 3: Cell-type-specific deletion of Bace1 alters the steady-state rate of Aβ production. | Nature Neuroscience

Fig. 3: Cell-type-specific deletion of Bace1 alters the steady-state rate of Aβ production.

From: Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer’s disease model mice

Fig. 3

a,b, Aβ electrochemiluminescence immunoassay data of insoluble (SDS-soluble, left) and soluble (Tris-NaCl-soluble, right) lysates of microdissected cortical (a) and WM (b) tissues from control and cKO 6-month-old male mouse hemibrains (n = 7 per group). Triplex immunoassay measured Aβ38, Aβ40 and Aβ42 levels, and data points were normalized to Control;AD samples. Of note, SDS-soluble fractions from both regions mirrored LSM data, whereas Tris-NaCl-soluble fractions revealed a substantial amount of soluble Aβ still being produced, even in ExN-Bace1cKO;AD mice, signifying a residual Aβ production from other cells. Statistical analysis: one-way ANOVA with Tukey multiple comparison tests (P values indicated in graphs with significance highlighted in bold). Bars represent means with s.e.m., and individual data points are displayed. Raw unnormalized data are available in Supplementary Table 6. c, Working model of modulating cell-type-specific Aβ contributions. Selectively ablating Aβ from specific cell types results in steady-state rate change of Aβ production, causing exponentially slower plaque growth that follows a sigmoidal growth curve. ctrl, control; rel., relative.

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