Although changes in LIMK1/cofilin signaling in animal models of AD appear to be complex being affected by subcellular compartments and age of the mice [25, 27, 30–33], increased cofilin activity as determined by decreased P-Cofilin and the formation of aberrant cofilin-actin rods (characterized by accumulation of active cofilin) are fairly consistent observations [25, 28–40]. This evidence concerns the gene CFL1 and Alzheimer disease.