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Study identifies new cellular mechanisms in multiple sclerosis

A pioneering study, carried out by a research team from the Andalusian Center for Developmental Biology (CABD), has identified key alterations in mitochondrial dysfunction, iron metabolism and inflammation in cells derived from patients with multiple sclerosis. Published in the scientific journal Aging, the work, led by Professor of Cell Biology at the Universidad Pablo de Olavide José Antonio Sánchez Alcázar, provides new insights into the cellular processes involved in this neurodegenerative disease and opens the door to possible innovative therapeutic strategies.

Multiple sclerosis is an inflammatory and demyelinating disease of the central nervous system that affects approximately 2.8 million people worldwide. Although effective treatments exist for the relapsing-remitting phase of the disease, therapeutic options for progressive forms remain limited, necessitating a better understanding of the mechanisms underlying its progression.

Key findings: mitochondrial dysfunction, iron metabolism and neuroinflammation

The research team analyzed fibroblasts (skin cells) obtained from patients with multiple sclerosis and found alterations in their cell morphology, with characteristics associated with senescence. In addition, they observed an accumulation of iron in the form of lipofuscin, a pigment associated with aging, as well as increased lipid peroxidation and reduced antioxidant enzymes, suggesting a state of elevated oxidative stress.

One of the most striking findings of the study is the high sensitivity of fibroblasts to ferroptosis, a type of iron-dependent cell death, suggesting that disruption in iron homeostasis may play a central role in disease progression. In addition, the research team identified activation of the inflammasome, a multiprotein complex involved in the inflammatory response, which could contribute to the chronic neuroinflammation observed in multiple sclerosis.


Summary of the key findings

Implications for future research and treatment.

Until now, multiple sclerosis has been considered primarily an autoimmune disease, in which the immune system itself attacks myelin, the coating that protects nerve fibers. However, this new study suggests that other cellular processes, such as iron metabolism and oxidative stress, also play a key role in the pathogenesis of the disease.

“These results change the paradigm of multiple sclerosis, as they show that not only the immune system is involved, but also that patients' own cells present intrinsic inflammatory mechanisms, which leads us to reconsider our approach in the search for new therapies,” explains José Antonio Sánchez Alcázar.

Thus, the study represents a significant step forward in the understanding of multiple sclerosis and highlights the importance of continuing to explore approaches beyond the autoimmune paradigm to tackle this complex disease.

Scientific work: García-Salas R, Cilleros-Holgado P, Di Spirito A, Gómez-Fernández D, Piñero-Pérez R, Romero-Domínguez JM, Álvarez-Córdoba M, Reche-López D, Romero-González A, López-Cabrera A, Sánchez-Alcázar JA. Mitochondrial dysfunction, iron accumulation, lipid peroxidation and inflammasome activation in cellular models derived from patients with multiple sclerosis. Aging, 2025. DOI: https://doi.org/10.18632/aging.206198