Mitochondrial Ca(2+) in neurodegenerative disorders

Abstract

Functional mitochondria are vital to accomplish their key role in the cell, by maintaining the energy metabolism, buffering of the Ca(2+) signal and directing the cell death mechanism. Mitochondrial Ca(2+) can stimulate ATP production or trigger the opening of mitochondrial permeability transition pore and activating the cell death cascade. Mitochondrial Ca(2+) uptake play a crucial role in neurons by buffering excessive Ca(2+) from the cytosol at the time of the transmission of the signal. Changes in the maintenance of mitochondrial Ca(2+) may trigger neuronal cell death. Abnormality in mitochondrial Ca(2+) handling has been detected in a range of neurodegenerative diseases, and emerging evidence from disease models suggests that mitochondrial Ca(2+) may play a role in disease pathogenesis. In this review, we assess how mitochondrial Ca(2+) imbalance may be a trigger in common neurodegenerative disease.

Keywords: Alzheimer's disease; Astrocyte; Calcium; Mitochondria; Neurodegeneration; Neurons; Parkinson's disease.