[1] Zarei S, Carr K, Reiley L, et al. A comprehensive review of amyotrophic lateral sclerosis [J]. Surg Neurol Int, 2015, 6(1): 171. [2] Kiernan MC, Vucic S, Cheah BC, et al. Amyotrophic lateral sclerosis [J]. Lancet, 2011, 377(9769): 942-955. [3] Swinnen B, Robberecht W. The phenotypic variability of amyotrophic lateral sclerosis [J]. Nat Rev Neurol, 2014, 10(11): 661-670. [4] Couthouis J, Raphael AR, Daneshjou R, et al. Targeted exon capture and sequencing in sporadic amyotrophic lateral sclerosis [J]. PLoS Genet, 2014, 10(10): e1004704. [5] Maruyama H, Morino H, Kawakami H. [Causative genes for amyotrophic lateral sclerosis] [J]. [in Japanese]. Brain Nerve, 2016, 68(9): 1081-1086. [6] Trias E, Ibarburu S, Barreto-Núñez R, et al. Significance of aberrant glial cell phenotypes in pathophysiology of amyotrophic lateral sclerosis [J]. Neurosci Lett, 2016, 636: 27-31. [7] Ayers JI, McMahon B, Gill S, et al. Relationship between mutant SOD1 maturation and inclusion formation in cell models [J]. J Neurochem, 2017, 140(1): 140-150. [8] Prudencio M, Hart PJ, Borchelt DR, et al. Variation in aggregation propensities among ALS-associated variants of SOD1: correlation to human disease [J]. Hum Mol Genet, 2009, 18(17): 3217-3226. [9] Chattopadhyay M, Nwadibia E, Strong CD, et al. The disulfide bond, but not zinc or dimerization, controls initiation and seeded growth in amyotrophic lateral sclerosis-linked Cu, Zn superoxide dismutase (SOD1) fibrillation [J]. J Biol Chem, 2015, 290(51): 30624-30636. [10] Ayers JI, Fromholt SE, O'Neal VM, et al. Prion-like propagation of mutant SOD1 misfolding and motor neuron disease spread along neuroanatomical pathways [J]. Acta Neuropathol, 2016, 131(1): 103-114. [11] Bruijn LI, Miller TM, Cleveland DW. Unraveling the mechanisms involved in motor neuron degeneration in ALS [J]. Annu Rev Neurosci, 2004, 27: 723-749. [12] Wang I, Wu LS, Chang HY, et al. TDP-43, the signature protein of FTLD-U, is a neuronal activity-responsive factor [J]. J Neurochem, 2008, 105(3): 797-806. [13] Gendron TF, Rademakers R, Petrucelli L. TARDBP mutation analysis in TDP-43 proteinopathies and deciphering the toxicity of mutant TDP-43 [J]. J Alzheimers Dis, 2013, 33(s1): S35-S45. [14] Lu Y, Tang C, Zhu L, et al. The overexpression of TDP-43 protein in the neuron and oligodendrocyte cells causes the progressive motor neuron degeneration in the SOD1 G93A transgenic mouse model of amyotrophic lateral sclerosis [J]. Int J Biol Sci, 2016, 12(9): 1140-1149. [15] Maruyama H, Kawakami H. Optineurin and amyotrophic lateral sclerosis [J]. Geriatr Gerontol Int, 2013, 13(3): 528-532. [16] Patai R, Nógrádi B, Engelhardt JI, et al. Calcium in the pathomechanism of amyotrophic lateral sclerosis-Taking center stage? [J]. Biochem Biophys Res Commun, 2017, 483(4): 1031-1039. [17] D'Amico E, Factor-Litvak P, Santella RM, et al. Clinical perspective on oxidative stress in sporadic amyotrophic lateral sclerosis [J]. Free Radical Bio Med, 2013, 65: 509-527. [18] Barber SC, Shaw PJ. Oxidative stress in ALS: key role in motor neuron injury and therapeutic target [J]. Free Radical Biol Med, 2010, 48(5): 629-641. [19] DeCoteau W, Heckman KL, Estevez AY, et al. Cerium oxide nanoparticles with antioxidant properties ameliorate strength and prolong life in mouse model of amyotrophic lateral sclerosis [J]. Nanomedicine, 2016, 12(8): 2311-2320. [20] Melachroinou K, Xilouri M, Emmanouilidou E, et al. Deregulation of calcium homeostasis mediates secreted α-synuclein-induced neurotoxicity [J]. Neurobiol Aging, 2013, 34(12): 2853-2865. [21] Kiselyov K, Muallem S. ROS and intracellular ion channels [J]. Cell Calcium, 2016, 60(2): 108-114. [22] Wuolikainen A, Moritz T, Marklund SL, et al. Disease-related changes in the cerebrospinal fluid metabolome in amyotrophic lateral sclerosis detected by GC/TOFMS [J]. PLoS One, 2011, 6(4): e17947. [23] Bonifacino T, Musazzi L, Milanese M, et al. Altered mechanisms underlying the abnormal glutamate release in amyotrophic lateral sclerosis at a pre-symptomatic stage of the disease [J]. Neurobiol Dis, 2016, 95: 122-133. [24] Milanese M, Zappettini S, Onofri F, et al. Abnormal exocytotic release of glutamate in a mouse model of amyotrophic lateral sclerosis [J]. J Neurochem, 2011, 116(6): 1028-1042. [25] Tani H, Dulla CG, Farzampour Z, et al. A local glutamate-glutamine cycle sustains synaptic excitatory transmitter release [J]. Neuron, 2014, 81(4): 888-900. [26] Vucic S, Rothstein JD, Kiernan MC. Advances in treating amyotrophic lateral sclerosis: insights from pathophysiological studies [J]. Trends Neurosci, 2014, 37(8): 433-442. [27] Rueda CB, Llorente-Folch I, Traba J, et al. Glutamate excitotoxicity and Ca 2+ -regulation of respiration: Role of the Ca 2+ activated mitochondrial transporters (CaMCs) [J]. Biochim Biophys Acta, 2016, 1857(8): 1158-1166. [28] Magrané J, Cortez C, Gan WB, et al. Abnormal mitochondrial transport and morphology are common pathological denominators in SOD1 and TDP43 ALS mouse models [J]. Hum Mol Genet, 2014, 23(6): 1413-1424. [29] Salehi M, Nikkhah M, Ghasemi A, et al. Mitochondrial membrane disruption by aggregation products of ALS-causing superoxide dismutase-1 mutants [J]. Int J Biol Macromol, 2015, 75: 290-297. [30] Israelson A, Arbel N, Da Cruz S, et al. Misfolded mutant SOD1 directly inhibits VDAC1 conductance in a mouse model of inherited ALS [J]. Neuron, 2010, 67(4): 575-587. [31] Sasaki S, Iwata M. Mitochondrial alterations in the spinal cord of patients with sporadic amyotrophic lateral sclerosis [J]. J Neuropathol Exp Neurol, 2007, 66(1): 10-16. [32] Liu W, Yamashita T, Tian F, et al. Mitochondrial fusion and fission proteins expression dynamically change in a murine model of amyotrophic lateral sclerosis [J]. Curr Neurovasc Res, 2013, 10(3): 222-230. [33] Palomo GM, Manfredi G. Exploring new pathways of neurodegeneration in ALS: the role of mitochondria quality control [J]. Brain Res, 2015, 1607: 36-46. [34] Cozzolino M, Carrì MT. Mitochondrial dysfunction in ALS [J]. Prog Neurobiol, 2012, 97(2): 54-66. [35] Meininger V. ALS, what new 144 years after Charcot? [J]. Arch Ital Biol, 2011, 149(1): 29-37. [36] Farina C, Aloisi F, Meinl E. Astrocytes are active players in cerebral innate immunity [J]. Trends Immunol, 2007, 28(3): 138-145. [37] Zürcher NR, Loggia ML, Lawson R, et al. Increased in vivo glial activation in patients with amyotrophic lateral sclerosis: Assessed with [11 C]-PBR28 [J]. Neuroimage Clin, 2015, 7: 409-414. [38] Wormser U, Mandrioli J, Vinceti M, et al. Reduced levels of alpha-1-antitrypsin in cerebrospinal fluid of amyotrophic lateral sclerosis patients: a novel approach for a potential treatment [J]. J Neuroinflammation, 2016, 13(1): 1-5. [39] Lu CH, Allen K, Oei F, et al. Systemic inflammatory response and neuromuscular involvement in amyotrophic lateral sclerosis [J]. Neurol Neuroimmunol Neuroinflamm, 2016, 3(4): e244. [40] Dahlke C, Saberi D, Ott B, et al. Inflammation and neuronal death in the motor cortex of the wobbler mouse, an ALS animal model [J]. J Neuroinflammation, 2015, 12(1): 1-11. [41] May C, Nordhoff E, Casjens S, et al. Highly immunoreactive IgG antibodies directed against a set of twenty human proteins in the sera of patients with amyotrophic lateral sclerosis identified by protein array [J]. PLoS One, 2014, 9(2): e89596. [42] Pagani MR, Gonzalez LE, Uchitel OD. Autoimmunity in amyotrophic lateral sclerosis: past and present [J]. Neurol Res Int, 2011, 2011: 497080. [43] Nardo G, Trolese MC, de Vito G, et al. Immune response in peripheral axons delays disease progression in SOD1 G93A mice [J]. J Neuroinflammation, 2016, 13(1): 261. [44] Orrell RW, Lane RJM, Ross M. A systematic review of antioxidant treatment for amyotrophic lateral sclerosis/motor neuron disease [J]. Amyotroph Lateral Scler, 2009, 9(4): 195-211. [45] Glass JD, Hertzberg VS, Boulis NM, et al. Transplantation of spinal cord-derived neural stem cells for ALS: Analysis of phase 1 and 2 trials [J]. Neurology, 2016, 87(4): 392-400. |