Artículos de revistas
Mitochondria and calcium regulation as basis of neurodegeneration associated with aging
Fecha
2018Registro en:
Frontiers in Neuroscience, Volumen 12, Issue JUL, 2018,
1662453X
16624548
10.3389/fnins.2018.00470
Autor
Müller, Marioly
Ahumada-Castro, Ulises
Sanhueza, Mario
González Billault, Christian
Court, Felipe A.
Cárdenas, César
Institución
Resumen
© 2018 Müller, Ahumada-Castro, Sanhueza, Gonzalez-Billault, Court and Cárdenas.Age is the main risk factor for the onset of neurodegenerative diseases. A decline of mitochondrial function has been observed in several age-dependent neurodegenerative diseases and may be a major contributing factor in their progression. Recent findings have shown that mitochondrial fitness is tightly regulated by Ca2+ signals, which are altered long before the onset of measurable histopathology hallmarks or cognitive deficits in several neurodegenerative diseases including Alzheimer's disease (AD), the most frequent cause of dementia. The transfer of Ca2+ from the endoplasmic reticulum (ER) to the mitochondria, facilitated by the presence of mitochondria-associated membranes (MAMs), is essential for several physiological mitochondrial functions such as respiration. Ca2+ transfer to mitochondria must be finely regulated because excess Ca2+ will disturb oxidative phosphorylation (OXPHOS), thereby increasing