Calcium, mitochondria, and the pathogenesis of ALS: The good, the bad, and the ugly

Frontiers in Cellular Neuroscience

Volumn , Issue OCT, 2013, Pages

  Jaiswal, Manoj Kumar ^a  

^a Uniformed Services University of the Health Sciences and the Walter Reed National Military Medical Center   (United States)

Author keywords

Amyotrophic lateral sclerosis; Calcium buffer; Calcium homeostasis dysregulation; Mitochondrial dysfunction; Motor neuron disease; Neurodegeneration; Selective vulnerability

Indexed keywords

CALCIUM; CALCIUM CHANNEL; COPPER ZINC SUPEROXIDE DISMUTASE; REACTIVE OXYGEN METABOLITE;

AMYOTROPHIC LATERAL SCLEROSIS; APOPTOSIS; CALCIUM HOMEOSTASIS; CALCIUM SIGNALING; CELL MEMBRANE DEPOLARIZATION; CELL STRUCTURE; EDITORIAL; GENE MUTATION; HUMAN; MITOCHONDRION; MOTONEURON; NERVE CELL NECROSIS; NERVE DEGENERATION; NEUROPATHOLOGY; NONHUMAN; OXIDATIVE STRESS;

EID: 84886812271     PISSN: 16625102     EISSN: None     Source Type: Journal    
DOI: 10.3389/fncel.2013.00199     Document Type: Editorial

References (3)

1. 2+ homeostasis in SOD1G93A mice. Mol. Pharmacol. 75, 478-489. doi: 10.1124/mol.108.050831
2. Jaiswal, M. K., Zech, W. D., Goos, M., Leutbecher, C., Ferri, A., Zippelius, A., et al. (2009). Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease. BMC Neurosci. 10:64. doi: 10.1186/1471-2202-10-64
3. 2+, mitochondria and selective motoneuron vulnerability: implications for ALS. Trends Neurosci. 28, 494-500. doi: 10.1016/j.tins.2005.07.001