title: 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.
authors.affiliation: Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
authors.forename: Rosella
authors.initials: R
authors.lastname: Abeti
authors.affiliation: Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK. Electronic address: a.abramov@ucl.ac.uk.
authors.forename: Andrey Y
authors.initials: AY
authors.lastname: Abramov
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D016923:Cell Death / Q000502:physiology; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D019636:Neurodegenerative Diseases / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism
chemical_list: D002118:Calcium
keywords: Alzheimer's disease; Astrocyte; Calcium; Mitochondria; Neurodegeneration; Neurons; Parkinson's disease