Alzheimer disease and calcium

Abstract

Calcium deficiency due to insufficient nutritional intake, poor intestinal absorption or excessive urinary loss leading to secondary hyperparathyroidism, increase of calcium influx into nerve cells causing cell death may lead to neuronal dysfunction and cell death as in dialysis encephalopathy with EEG changes and decrease of nerve conduction velocity in chronic renal failure and Alzheimer's disease in aging. Intracellular free calcium (Ca i) is increased in nerve cells showing neurofibrillar tangles associated with tau protein in Alzheimer's disease. Increase of Ca i facilitates presenilin mutation with consequent augmentation of short chain amyloid beta production which further increase Ca i. Peroxide radical production by amyloid beta and metals such as Fe, Cu and Mn is prompted by an increase of Ca i. Plasma membrane damage caused by lipid peroxidation further increases Ca i. Neurotoxic action of apolipoprotein E(4) increasing the risk for Alzheimer's disease may be explained by lipid peroxidation and rise of Ca i. Beneficial effect of estrogen in preventing Alzheimer's disease may also be explained by its anti-oxidant effect and stimulation of intestinal calcium absorption. By increasing calcium intake and administration of active form of vitamin D which cannot be sufficiently supplied by the aging kidney, one step forward should be made in the prevention and treatment of Alzheimer's disease.