**Author details**

Maria Teresa Gonzalez Garza

Address all correspondence to: mtgonzalezgarza@itesm.mx

School of Medicine, Tecnologico de Monterrey, Monterrey, Mexico

#### **References**

lament), the cytochrome *c* oxidase gene, and protein of the nuclear membrane NAV3 and

Other cells that contribute to the disease are microglia cells, lymphocytes, and Schwann cells [89–91]. A recent hypothesis is that Schwann and muscle cells are also direct partners of the injured motor axons and may respectively be the recipients or initiators of the initial damage

In a mice ALS model, it has been proved that miR-365 and miR-125b suppress the IL-6/STAT3 pathway in microglia cells with an increase in the levels of TNFα mRNA [93]. This agrees with the fact that TNFα is upregulated in G93A mice and ALS patients [94, 95], which indicates that miR-365 and miR-125b dysregulations might develop the pathological cytokine profile on ALS.

Until now, there is no consensus on which miRNA could be the best target for therapy. To alter the cell homeostasis of miRNAs, more than one change is needed for their biogenesis. Similar to previous reports, miRNA can have several target mRNAs and one mRNA can be regulated by different microRNAs. ALS research provides an example of NEFL synthesis alteration, which can be regulated by miR-b2403, miR-b1336, miR-146a, miR-524-5p, and miR-582-3p. Probably, for the development of diseases, the coincidence of more than one dysregulation is necessary, or the accumulative alteration of various changes in the transcriptome, to induce neuron cell death. On the other hand, the dysregulation of miRNAs on neighbor cells partic‐ ipates in ALS pathology, where microglia cells, lymphocytes, Schwann cells, and muscle cells show a dysregulation in the miRNA transcript. Further, miRNAs also participate in neuron death. Nevertheless, research on miRNAs involves looking at miRNAs from the perspective of biomarkers. Moreover, the systematic comparative analysis of their profile between healthy people and ALS patients provides information on which pathways can be suggested as possible targets for directed therapy. In addition, the analysis also provides an opportunity to know more about the development of this disease, metabolic pathways altered, and cells

related neuronal regeneration.

126 Update on Amyotrophic Lateral Sclerosis

[67, 92].

**11. Conclusion**

involved in ALS pathology.

Maria Teresa Gonzalez Garza

Address all correspondence to: mtgonzalezgarza@itesm.mx

School of Medicine, Tecnologico de Monterrey, Monterrey, Mexico

**Author details**


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