Age-related macular degeneration(AMD)is a common eye disease causing irreversible visual impairment in the elderly. The tight junction(TJ)between retinal pigment epithelium cells(RPECs)is an important structural unit of the outer blood retinal barrier(oBRB). The TJ is defective in the pathogenesis of AMD, which in turn promotes the destruction of oBRB and accelerates the occurrence and progression of AMD. In this paper, the roles of TJ and TJ protein in maintaining oBRB function, TJ protein abnormality and oBRB destruction in the pathogenesis of AMD were reviewed, aiming to provide new ideas for the treatment of AMD.