[1] Hardiman O, van den Berg LH, Kiernan MC. Clinical diagnosis and management of amyotrophic lateral sclerosis. Nat Rev Neurol, 2011; 7, 639−49.
[2] Mancuso R, Navarro X. Amyotrophic lateral sclerosis: current perspectives from basic research to the clinic. Prog Neurobiol, 2015; 133, 1−26. doi:  10.1016/j.pneurobio.2015.07.004
[3] Oggiano R, Pisano A, Sabalic A, et al. An overview on amyotrophic lateral sclerosis and cadmium. Neurol Sci, 2021; 42, 531−7. doi:  10.1007/s10072-020-04957-7
[4] Wang MD, Little J, Gomes J, et al. Identification of risk factors associated with onset and progression of amyotrophic lateral sclerosis using systematic review and meta-analysis. Neurotoxicology, 2017; 61, 101−30. doi:  10.1016/j.neuro.2016.06.015
[5] Westeneng HJ, Debray TPA, Visser AE, et al. Prognosis for patients with amyotrophic lateral sclerosis: development and validation of a personalised prediction model. Lancet Neurol, 2018; 17, 423−33. doi:  10.1016/S1474-4422(18)30089-9
[6] Ahuja A, Dev K, Tanwar RS, et al. Copper mediated neurological disorder: visions into amyotrophic lateral sclerosis, Alzheimer and Menkes disease. J Trace Elem Med Biol, 2015; 29, 11−23. doi:  10.1016/j.jtemb.2014.05.003
[7] Tokuda E, Furukawa Y. Copper homeostasis as a therapeutic target in amyotrophic lateral sclerosis with SOD1 mutations. Int J Mol Sci, 2016; 17, 636. doi:  10.3390/ijms17050636
[8] Oggiano R, Solinas G, Forte G, et al. Trace elements in ALS patients and their relationships with clinical severity. Chemosphere, 2018; 197, 457−66. doi:  10.1016/j.chemosphere.2018.01.076
[9] Tesauro M, Bruschi M, Filippini T, et al. Metal(loid)s role in the pathogenesis of amyotrophic lateral sclerosis: environmental, epidemiological, and genetic data. Environ Res, 2021; 192, 110292. doi:  10.1016/j.envres.2020.110292
[10] Peters S, Broberg K, Gallo V, et al. Blood metal levels and amyotrophic lateral sclerosis risk: a prospective cohort. Ann Neurol, 2021; 89, 125−33. doi:  10.1002/ana.25932
[11] Qin X, Wu P, Wen T, et al. Comparative assessment of blood Metal/metalloid levels, clinical heterogeneity, and disease severity in amyotrophic lateral sclerosis patients. Neurotoxicology, 2022; 89, 12−9. doi:  10.1016/j.neuro.2022.01.003
[12] Petri S, Calingasan NY, Alsaied OA, et al. The lipophilic metal chelators DP-109 and DP-460 are neuroprotective in a transgenic mouse model of amyotrophic lateral sclerosis. J Neurochem, 2007; 102, 991−1000. doi:  10.1111/j.1471-4159.2007.04604.x
[13] Hottinger AF, Fine EG, Gurney ME, et al. The copper chelator d-penicillamine delays onset of disease and extends survival in a transgenic mouse model of familial amyotrophic lateral sclerosis. Eur J Neurosci, 1997; 9, 1548−51. doi:  10.1111/j.1460-9568.1997.tb01511.x
[14] Andreassen OA, Dedeoglu A, Klivenyi P, et al. N-acetyl-L-cysteine improves survival and preserves motor performance in an animal model of familial amyotrophic lateral sclerosis. Neuroreport, 2000; 11, 2491−3. doi:  10.1097/00001756-200008030-00029
[15] Peters TL, Beard JD, Umbach DM, et al. Blood levels of trace metals and amyotrophic lateral sclerosis. Neurotoxicology, 2016; 54, 119−26. doi:  10.1016/j.neuro.2016.03.022
[16] Brooks BR, Miller RG, Swash M, et al. El Escorial revisited: revised criteria for the diagnosis of amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord, 2000; 1, 293−9. doi:  10.1080/146608200300079536
[17] Cedarbaum JM, Stambler N, Malta E, et al. The ALSFRS-R: a revised ALS functional rating scale that incorporates assessments of respiratory function. BDNF ALS Study Group (Phase III). J Neurol Sci, 1999; 169, 13−21. doi:  10.1016/S0022-510X(99)00210-5
[18] Goutman SA. Diagnosis and clinical management of amyotrophic lateral sclerosis and other motor neuron disorders. Continuum (Minneap Minn), 2017; 23, 1332−59.
[19] Hou HL, Wang LW, Fu TY, et al. Magnesium acts as a second messenger in the regulation of NMDA receptor-mediated CREB signaling in neurons. Mol Neurobiol, 2020; 57, 2539−50. doi:  10.1007/s12035-020-01871-z
[20] Hemerková P, Vališ M. Role of oxidative stress in the pathogenesis of amyotrophic lateral sclerosis: antioxidant metalloenzymes and therapeutic strategies. Biomolecules, 2021; 11, 437. doi:  10.3390/biom11030437
[21] Zheltova AA, Kharitonova MV, Iezhitsa IN, et al. Magnesium deficiency and oxidative stress: an update. Biomedicine (Taipei), 2016; 6, 20. doi:  10.7603/s40681-016-0020-6
[22] Wang QQ, Liu YJ, Zhou JW. Neuroinflammation in Parkinson's disease and its potential as therapeutic target. Transl Neurodegener, 2015; 4, 19. doi:  10.1186/s40035-015-0042-0
[23] Redler RL, Dokholyan NV. The complex molecular biology of amyotrophic lateral sclerosis (ALS). Prog Mol Biol Transl Sci, 2012; 107, 215−62.
[24] Fondell E, O'Reilly ÉJ, Fitzgerald KC, et al. Magnesium intake and risk of amyotrophic lateral sclerosis: results from five large cohort studies. Amyotroph Lateral Scler Frontotemporal Degener, 2013; 14, 356−61. doi:  10.3109/21678421.2013.803577
[25] Yase Y, Yoshida S, Kihira T, et al. Kii ALS dementia. Neuropathology, 2001; 21, 105−9. doi:  10.1046/j.1440-1789.2001.00303.x
[26] Koski L, Berntsson E, Vikström M, et al. Metal ratios as possible biomarkers for amyotrophic lateral sclerosis. J Trace Elem Med Biol, 2023; 78, 127163. doi:  10.1016/j.jtemb.2023.127163
[27] Tainer JA, Getzoff ED, Beem KM, et al. Determination and analysis of the 2 Å structure of copper, zinc superoxide dismutase. J Mol Biol, 1982; 160, 181−217. doi:  10.1016/0022-2836(82)90174-7
[28] Arnesano F, Banci L, Bertini I, et al. The unusually stable quaternary structure of human Cu, Zn-superoxide dismutase 1 is controlled by both metal occupancy and disulfide status. J Biol Chem, 2004; 279, 47998−8003. doi:  10.1074/jbc.M406021200
[29] Sannigrahi A, Chowdhury S, Das B, et al. The metal cofactor zinc and interacting membranes modulate SOD1 conformation-aggregation landscape in an in vitro ALS model. Elife, 2021; 10, e61453. doi:  10.7554/eLife.61453
[30] Dashnaw CM, Zhang AY, Gonzalez M, et al. Metal migration and subunit swapping in ALS-linked SOD1: Zn2+ transfer between mutant and wild-type occurs faster than the rate of heterodimerization. J Biol Chem, 2022; 298, 102610. doi:  10.1016/j.jbc.2022.102610
[31] Coussee E, De Smet P, Bogaert E, et al. G37R SOD1 mutant alters mitochondrial complex I activity, Ca2+ uptake and ATP production. Cell Calcium, 2011; 49, 217−25. doi:  10.1016/j.ceca.2011.02.004
[32] Ferrè S, Hoenderop JGJ, Bindels RJM. Sensing mechanisms involved in Ca2+ and Mg2+ homeostasis. Kidney Int, 2012; 82, 1157−66. doi:  10.1038/ki.2012.179
[33] Chang Q, Martin LJ. Voltage-gated calcium channels are abnormal in cultured spinal motoneurons in the G93A-SOD1 transgenic mouse model of ALS. Neurobiol Dis, 2016; 93, 78−95. doi:  10.1016/j.nbd.2016.04.009
[34] Yasui M, Yase Y, Kihira T, et al. Magnesium and calcium contents in CNS tissues of amyotrophic lateral sclerosis patients from the Kii peninsula, Japan. Eur Neurol, 1992; 32, 95−8. doi:  10.1159/000116800
[35] Guo L, Mao QL, He J, et al. Disruption of ER ion homeostasis maintained by an ER anion channel CLCC1 contributes to ALS-like pathologies. Cell Res, 2023; 33, 497−515. doi:  10.1038/s41422-023-00798-z
[36] Peggion C, Scalcon V, Massimino ML, et al. SOD1 in ALS: taking stock in pathogenic mechanisms and the role of glial and muscle cells. Antioxidants (Basel), 2022; 11, 614. doi:  10.3390/antiox11040614
[37] Zhou CN, Li M, Xiao R, et al. Significant nutritional gaps in tibetan adults living in agricultural counties along Yarlung Zangbo river. Front Nutr, 2022; 9, 845026. doi:  10.3389/fnut.2022.845026
[38] Su CH, Wang JW, Chen ZW, et al. Sources and health risks of heavy metals in soils and vegetables from intensive human intervention areas in South China. Sci Total Environ, 2023; 857, 159389. doi:  10.1016/j.scitotenv.2022.159389
[39] Wang YY, Li DD, Xu KF, et al. Copper homeostasis and neurodegenerative diseases. Neural Regen Res, 2025; 20, 3124−43. doi:  10.4103/NRR.NRR-D-24-00642