The inhibition of cofilin dephosphorylation in the Familial Autosomal dominant (FAD) mouse model of AD that express several pathogenic mutations in APP and Presinilin1 genes, decreases Aβ plaques, cellular defects and improves cognitive function, confirming the link between Aβ pathologies and actin cytoskeleton (Deng et al., 2016). This evidence concerns the gene CFL1 and Alzheimer disease.