Aging, dementia and calcium metabolism

Summary

After a brief discussion of the theory of disturbed neuronal calcium metabolism an overview is given on the results of clinical studies with nimodipine in the treatment of vascular and Alzheimer’s dementia.

Calcium seems to be the essential if not the only intracellular signal transmitter, on which all the signals transduced by the different transmitter systems converge, modulating the intracellular calcium concentration. Secondly disturbance to the intracellular calcium homeostasis is the common mechanism by which noxious interventions, like for instance hypoxia, deteriorate cell function, and finally even lead to cell death. There have been many experimental data showing that the ability of cells to sustaine calcium homeostasis might be impaired by the aging process itself. The hypothesis has been postulated, that this impairment might also be of central importance for brain aging, associated cognitive decline and development of dementia. In that sense the age dependent increasing incapacitation of the intraneuronal calcium regulating processes could be viewed as risk factors causing the increasing susceptibility of brain cells against any noxious agents including etiology of dementia in general and Alzheimer’s dementia in particular. Khachaturian (1989) has argued that a longlasting continuous and rather small impairment of calcium homeostasis may have the same effect as an acute and massive calcium overloading of neuronal cells as for example induced by acute ischemic states.