Alzheimer Disease may result from excessive stimulation of the innate immune system from development of underlying opportunistic infections and impaired age related self recognition as non-self, due to immunodeficiency and immunosenescence, resulting in excessive inflammation and runaway Beta-amyloid production (a component of the innate immune system) causing cytosolic calcium overload. Excessive cytosolic calcium may cause over activation of calcineurin and inactivation of cis-trans prolyl isomerase (Pin1), with subsequent loss of dendritic spine maintenance, and synaptic destruction. Improving immune function, identifying and treating infections, avoiding runaway Beta-amyloid production and inhibiting calcineurin in a manner similar to that utilized in preventing tissue transplant rejection, may lead to improved prevention and treatment of Alzheimer Disease.