Review of the literature reveals that several biochemical events implicated in the pathology of Alzheimer's disease (AD) are calcium dependent processes. These processes include normal processing of β-amyloid precursor protein, dephosphorylation and degradation of tau, neurotransmitter release and memory formation. Since all of these processes appear to be inactivated during progression of AD, we propose that a "deficit" of intracellular calcium levels may occur in the early phase of the disease. We also propose several experiments to test this hypothesis. The hypothesis predicts that presenilins most likely act as calcium channels in vivo and that their gene mutations may cause the disease by diminishing the Ca²⁺ channeling function.