On the other hand, deficits in synaptic plasticity in the AD progression are also linked with the active/dephosphorylated species of cofilin-1 which aggregate into aberrant cofilin-actin rods, leading eventually to an axonal trafficking jam, blockage of intracellular transport of mitochondria, loss of dendritic spines and synapse starvation [170,171,172,173,174]. This evidence concerns the gene CFL1 and Alzheimer disease.