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However, therapies targeting these molecules have shown contradictory results, underscoring the need for further research to find effective treatments.25–27 Autoimmunity Genetic evidence supports the autoimmune hypothesis as the main mechanism of vitiligo, with approximately 85% of susceptibility genes involved in innate, adaptive immunity, and apoptosis.4,28 This theory is also reinforced by the relationship of vitiligo with other autoimmune disorders, the presence of specific antibodies in patients, and the use of immunomodulatory therapies.4,28 Furthermore, it has been observed that treatments with immune checkpoint inhibitors in cancer patients can induce the development of vitiligo, suggesting a link between autoimmunity and this disease.29 Autoimmune diseases are the main comorbidity associated with vitiligo, including thyroid disorders, pernicious anemia, alopecia areata, connective tissue diseases, among others.30,31 Zombie cells, senescent cells in vitiligo Cellular senescence is induced in response to cellular stressors
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Memantine can provide useful day-to-day glutamate control Memantine is a low-affinity NMDA receptor antagonist that may reduce excessive receptor activation without broadly shutting down normal glutamate function
