CFL1 and Alzheimer disease: For example, Rush et al. observed an increase in Cofilin phosphorylation in mice models and AD patients, which led to synaptic plasticity loss and synaptotoxicity by inducing abnormal Actin stabilization, demonstrating that this could be a result of Rho-associated protein kinase (ROCK) pathway activation in concert with Aβ cellular exposure (Figure 3d) [174].