An overview of the pathophysiology and the past, current, and future treatments of neovascular age-related macular degeneration

Abstract

Age-related macular degeneration (AMD) is the leading cause of blindness in elderly people in New Zealand and other developed countries. Neovascular AMD has a rapid onset and can lead to an overall loss of independence. Patients often present with an absolute central scotoma and distortion. The pathophysiology of neovascular AMD is thought to be associated with polymorphisms and mutations in genes which are involved with the progression of the complement cascade. Vascular endothelial growth factor (VEGF) may contribute to the progression of AMD via excessive angiogenesis and permeability of vessels associated with the retina. Current treatments for neovascular AMD act to reduce pathological angiogenesis via multiple mechanisms. Bevacizumab and ranibizumab bind to VEGF receptor 2 (VEGFR2), suppressing the actions of VEGF-A. Similar drugs, such as aflibercept, bind to placental growth factor (PIGF) in addition to VEGFR2, triggering similar effects. Endeavours to improve current treatments such as the safer use of brolucizumab and the use of the port delivery system for ranibizumab are being researched to maximise efficiency of therapies, to meet increasing demand. There are many direct and indirect costs of AMD on patients and hospitals. With an ageing population who suffer from more comorbidities, AMD cases are expected to rise; we must therefore endeavour to improve existing treatments, and future techniques for management should not be discarded without serious consideration.