Additionally, a study designed to identify binding partners, which recruit CK1 to Alzheimer’s disease (AD) ubiquitinated lesions identified a dysbindin structural homolog that interacts with CK1γ, δ, and ε, and in the case of CK1δ it has been shown to be a concentration-dependent inhibitor (194). This evidence concerns the gene DTNBP1 and Alzheimer disease.