CALD1 participates in Ca2+-dependent intracellular trafficking, and its upregulation stabilizes actin filaments that impair cell migration/invasion (Castellino et al., 1992; Mukhopadhyay et al., 2009), breakdown of the tight junction that can be correlated with the loss of synaptic markers in AD (Zheng et al., 2004; Yamazaki et al., 2019), and stresses fiber formation (Mayanagi et al., 2008). Here, CALD1 is linked to Alzheimer disease.