Vitiligo is a common skin disorder with an estimated prevalence of 1-2% of the world population. It is characterised by well demarcated milky white patches of depigmentation which have the tendency to enlarge and spread peripherally. The pathogenesis is not fully understood, a process leads and end in the loss of functional melanocytes from the epidermis. There are many proposed theories and hypotheses, none of which can fully explain its pathogenesis. However, lately it is believed that an overlap between some of these theories can present better understanding. This is to include the two long standing theories i.e., the autoimmune and the neuronal. The latter been proposed in 1959, initially based on clinical observations and studies, including animal, physiological, biochemical, embryonic, structural and electron microscopy. In 1994 new evidence emerged linking the neuronal theory to autoimmune mechanisms by demonstration of changes in Neuropeptides in particular Neuropeptide Y (NPY), in the skin at the active edge of vitiligo skin. This review paper highlights all evidence supportive of the neuronal theory in the pathogenesis of vitiligo past and present.
Enhancing interfacial charge transfer in mesoporous MoS2/CdS nanojunction architectures for highly efficient visible-light photocatalytic water splitting
