Figure 1

Squalestatin increased the degradation of Aβ ₄₂ . (A) Immunoblot showing amyloid-beta (Aβ) monomers (M), dimers (D), and trimers (T) in conditioned media from 7PA2 cells (7PA2-CM) (1) and in Aβ-depleted 7PA2-CM (2). (B) Aβ monomers, dimers, and trimers eluted from a Superdex 75 PC column (separates proteins ranging from 3 to 70 kDa) loaded with concentrated 7PA2-CM. Values are mean Aβ₄₂ of duplicates. (C) Neurons were pre-treated with control medium (●) or 200 nM squalestatin (○), pulsed with 7PA2-CM containing 10 nM Aβ₄₂, and incubated for 1 to 5 days as shown. Values are mean Aβ₄₂ remaining in neurons ± standard deviation (SD) from triplicate experiments performed four times (n = 12). (D) Neurons were pre-treated with control medium (●) or 200 nM squalestatin (○), pulsed with 100 nM synthetic Aβ₄₂, and incubated for 1 to 5 days as shown. Values are mean Aβ₄₂ in neurons ± SD from triplicate experiments performed four times (n = 12). (E) Neurons were pre-treated with control medium (■) or 200 nM squalestatin (□) and pulsed with 7PA2-CM containing Aβ₄₂ as shown for 2 hours. Values are mean neuronal Aβ₄₂ ± SD from triplicate experiments performed three times (n = 9). (F) Neurons, incubated with 7PA2-CM containing 10 nM Aβ₄₂ for 2 days, were treated with control medium (■) or 200 nM squalestatin (□) for 24 hours. Values are the mean Aβ₄₂ remaining in neurons ± SD from triplicate experiments performed three times (n = 9). *Concentrations of Aβ₄₂ significantly less (P <0.05) than controls.