Calcium dysregulation, mitochondrial pathology and protein aggregation in a culture model of amyotrophic lateral sclerosis: Mechanistic relationship and differential sensitivity to intervention

►Increased Ca2+ in mitochondria, ER and cytoplasm preceded SOD1G93A inclusions. ►Increased cytosolic Ca2+ promoted SOD1G93A inclusion formation. ►Proteasome inhibition caused mitochondrial abnormalities, but independent of Ca2+. ►Geldanamycin prevented inclusions and mitochondrial rounding, but not altered Ca2+.