Fig. 6. ApoE modulates the toxicity of Aβ aggregates isoform-dependently.

A, B Permeabilization of lipid bilayers by early-stage (t₁) and fibrillar (t₃) Aβ aggregates ([Aβ42] = 4 µM in monomer equivalents; [apoE] = 0 or 80 nM). Ca²⁺ influx is referenced to the influx caused by the ionophore, ionomycin. C, D Neurotoxicity of t₁ and t₃ aggregates to human neuroblastoma SH-SY5Y cells, assayed by lactate dehydrogenase (LDH) release ([Aβ42] = 4 µM in monomer equivalents; [apoE] = 0 or 80 nM). Data points represent one of three independent experiments (B) or one of three or four biological replicates (D); error bars represent mean values +/− standard deviation of three independent (C) or four biological (D) replicates. Statistical significance was calculated using a unpaired two-sample t-test. *P < 0.05, **P < 0.01, ***P < 0.001, ns, non-significant (P ≥ 0.05). Source data are provided as a Source Data file.