Aberrant neuronal morphologies induced by TgCM or APP overexpression are prevented by Aβ depletion. A, Primary cultures were maintained in TgCM for 21 DIV in different culture conditions, as indicated. The percentage of neurons with dendritic dystrophies at 21 DIV is increased in the presence of TgCM, and this beading can be prevented by immunodepletion of Aβ. B, C, Representative GFP-labeled mature neurons (B) and Sholl analysis of branching on dendrites of neurons from indicated conditions shows that TgCM reduced branching and that this is rescued by immunodepletion of Aβ with 3D6 (C). D, Spine densities are determined in neurons without apparent dystrophies in each experimental condition, showing a decrease in spine density with TgCM that could be rescued with 3D6 treatment. E–H, Aβ depletion prevents APP overexpression-induced morphological abnormalities. In Tg cultures at 21 DIV, dendritic dystrophies (E), dendritic attenuation (F, G) and spine loss (H) are prevented by Aβ depletion with 3D6. Sixty cells were analyzed per experimental condition in each experiment. *p < 0.05; **p < 0.01; *p < 0.05 in G (Tg with 3D6 vs Tg with boiled 3D6). Data represent mean ± SD.