Neurodegeneration across species: analysis of the differences between canine degenerative myelopathy and human amyotrophic lateral sclerosis

Abstract

Amyotrophic lateral sclerosis (ALS) and canine degenerative myelopathy (DM) are highly complex neurodegenerative diseases characterized by progressive motor impairment and associated with mutations in the SOD1 gene, sharing common genetic mechanisms. This review analyzed, from a translational perspective, recent therapeutic advances in DM with potential application to ALS. The findings demonstrate that the aggregation of mutant SOD1 protein plays a central role in neuronal degeneration and is influenced by factors such as microRNAs, protein structural instability, and cell-to-cell propagation. Promising therapeutic strategies include gene modulation, enhancement of macrophage migration inhibitory factor (MIF) activity, the use of mesenchymal stem cells, and curcumin, all of which have shown potential to slow disease progression and improve quality of life. DM stands out as an important natural model for the development of new therapies for ALS.