Recent developments point to a critical role for calcium dysregulation in the pathogenesis of Alzheimer's disease. A novel calcium-conducting channel called CALHM1 is genetically linked to the disorder and modulates Aβ production. Calcium homeostasis has also been shown to be perturbed in dendritic spines adjacent to amyloid plaques. Finally, new studies have elucidated the role by which presenilins modulate calcium signaling, including effects on SERCA2b and gating of the IP3 receptor, and lead to Aβ production.
