In our case, Aβ-challenged neurons, although replicating, did not increase the expression and release of Cxcl1, one of the endogenous inflammatory chemokines that were associated with the appearance of senescence in cycling ALS neurons [14] and that we have selected because it has been linked to tau hyperphosphorylation [25]. This evidence concerns the gene CXCL1 and amyotrophic lateral sclerosis.