Spine pathology has been implicated in the early onset of Alzheimer & x2019;s disease (AD), where A & x3b2;-Oligomers (A & x3b2;Os) cause synaptic dysfunction and loss. Previously, we described that pharmacological inhibition of c-Abl prevents A & x3b2;Os-induced synaptic alterations. Hence, this kinase seems to be a key element in AD progression. Here, we studied the role of c-Abl on dendritic spine morphological changes induced by A & x3b2;Os using c-Abl null neurons (c-Abl-KO). First, we characterized the effect of c-Abl deficiency on dendritic spine density and found that its absence increases dendritic spine density. While A & x3b2;Os-treatment reduces the spine number in both wild-type (WT) and c-Abl-KO neurons, A & x3b2;Os-driven spine density loss was not affected by c-Abl. We then characterized A & x3b2;Os-induced morphological changes in dendritic spines of c-Abl-KO neurons. A & x3b2;Os induced a decrease in the number of mushroom spines in c-Abl-KO neurons while preserving the populations of immature stubby, thin, and filopodia spines. Furthermore, synaptic contacts evaluated by PSD95/Piccolo clustering and cell viability were preserved in A & x3b2;Os-exposed c-Abl-KO neurons. In conclusion, our results indicate that in the presence of A & x3b2;Os c-Abl participates in synaptic contact removal, increasing susceptibility to A & x3b2;Os damage. Its deficiency increases the immature spine population reducing A & x3b2;Os-induced synapse elimination. Therefore, c-Abl signaling could be a relevant actor in the early stages of AD.