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This review examines alopecia areata's pathophysiology, treatment options, and its significant psychosocial impact.
Alopecia areata [AA] is a chronic, immune-mediated hair loss disorder affecting approximately 2% of the global population across all ages, sexes, and ethnicities [1,2] It is driven by a collapse of immune privilege at the hair follicle, mediated primarily by autoreactive CD8+ T cells and the JAK-STAT signaling pathway.[3,4] Clinically, AA gifts as well-demarcated, non-scarring patches of hair loss that may development to total scalp hair loss [alopecia totalis] or complete body hair loss [alopecia universalis].[5] Diagnosis is predominantly clinical, supported by dermoscopy and, in uncertain cases, histopathology. Treatment has been historically limited but has undergone a paradigm shift with the FDA approval of JAK inhibitors—baricitinib [2022] and ritlecitinib [2023]—representing the first disease-modifying therapies for this condition.[6,7] Beyond clinical manifestations, AA imposes a significant psychosocial burden, with high rates of depression, anxiety, and impaired quality of life.[8,9]. This review manufactures current knowledge on the epidemiology, immunopathogenesis, diagnostic approaches, therapeutic landscape, and psychosocial dimensions of AA, with emphasis on emerging research directions.
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Vats et al. (2026) studied this question.