Age-related macular degeneration (AMD) is the leading cause of irreversible vision loss in older adults. Thyroid hormones are important regulators of development and metabolism, and a growing body of research suggests a role in the pathogenesis of AMD. Experimental studies have shown that excessive thyroid hormone signaling exacerbates oxidative stress, mitochondrial dysfunction, and cell death in the retina, while its inhibition confers protection in animal models of dry AMD. Genetic analyzes demonstrated that genetically predicted higher free thyroxine (FT4) is associated with an increased risk of AMD (OR 1.19, 95% CI 1.06–1.33), while no causal association was established for thyroid-stimulating hormone (TSH). Large population studies, including the Rotterdam Study, have consistently confirmed a positive association between blood FT4 levels and the incidence of AMD. The article summarizes progress from experimental, genetic and clinical studies on the relationship between thyroid hormones and AMD and highlights the biological mechanisms of this association.