CLOCK and neurodegenerative disease: Additionally, our work demonstrating rescue of pathology, memory deficits, and circadian dysfunction in a mouse model of beta-amyloidosis by inhibiting CK1 activity suggests that targeting post-translational mechanisms is also a viable strategy – especially since kinases, such as CK1, that work on both pathogenic and clock mechanisms act as a nexus between the two processes, which potentially addresses the neurodegenerative disease pathogenesis and circadian dysfunction simultaneously.