Alzheimer's disease (AD) is a fatal neurodegenerative disorder that has no known cure, nor is there a clear mechanistic understanding of the disease process itself. Although amyloid plaques, neurofibrillary tangles, and cognitive decline are late-stage markers of the disease, it is unclear how they are initially generated, and if they represent a cause, effect, or end phase in the pathology process. Recent studies in AD models have identified marked dysregulations in calcium signaling and related downstream pathways, which occur long before the diagnostic histopathological or cognitive changes. Under normal conditions, intracellular calcium signals are coupled to effectors that maintain a healthy physiological state. Consequently, sustained up-regulation of calcium may have pathophysiological consequences. Indeed, upon reviewing the current body of literature, increased calcium levels are functionally linked to the major features and risk factors of AD: ApoE4 expression, presenilin and APP mutations, beta amyloid plaques, hyperphosphorylation of tau, apoptosis, and synaptic dysfunction. In turn, the histopathological features of AD, once formed, are capable of further increasing calcium levels, leading to a rapid feed-forward acceleration once the disease process has taken hold. The views proposed here consider that AD pathogenesis reflects long-term calcium dysregulations that ultimately serve an enabling role in the disease process. Therefore, "Calcinists" do not necessarily reject betaAptist or Tauist doctrine, but rather believe that their genesis is associated with earlier calcium signaling dysregulations.