Fig. 6

DesAb-O prevents neuronal dysfunction induced by the CSFs of AD patients. A Intracellular Ca²⁺-derived fluorescence in SH-SY5Y cells treated for 5 h with ADDLs at 1 µM (monomer equivalents), or with CSFs from AD patients and age-matched control subjects (n = 4), diluted 1:1 with the extracellular medium, following 1 h pre-incubation in the absence or presence of DesAb-O at 3 µM. B Intracellular Ca²⁺-derived fluorescence in primary rat cortical neurons treated for 2.5 h with CSFs from AD patients and control subjects (n = 4), diluted 1:1 with the extracellular medium, following 1 h pre-incubation in the absence or presence of DesAb-O at 3 µM. C Intracellular calcein-derived fluorescence in SH-SY5Y cells treated for 5 h with ADDLs at 1 µM (monomer equivalents), or with CSFs from AD patients and control subjects (n = 4), diluted 1:1 with the extracellular medium, following 1 h pre-incubation in the absence or presence of DesAb-O at 3 µM. In all panels, untreated cells are also shown. D MTT reduction in SH-SY5Y cells treated for 24 h with ADDLs at 1 µM (monomer equivalents), or with CSFs from AD patients and control subjects (n = 4), diluted 1:1 with the extracellular medium, following 1 h pre-incubation in the absence or presence of DesAb-O at 3 µM. Experimental errors are S.E.M. Samples were analysed by Student t test relative to untreated cells (*P < 0.05, **P < 0.01 and ***P < 0.001) or to cells treated with samples without DesAb-O (§P < 0.05, §§P < 0.01 and §§§P < 0.001) or to cells treated with control CSFs (°P < 0.05 and °°P < 0.01). 200–250 (A,C), 80–150 (B) and 250,000–300,000 (D) cells were analysed per condition