AMD is the leading cause of severe vision loss in people over the age of 65 in the United States and other Western countries.³ It is characterized by a progressive degeneration of the central retina associated with central vision loss.²

Geographic atrophy is the “dry” form of the late stage of age-related macular degeneration (AMD).¹⁰ (You may also hear people refer to this condition as dry macular degeneration.) As the “dry” form of AMD progresses, cells in the light-sensitive portion of the macula, as well as the cells in the supporting structures (the retinal pigment epithelium and the choriocapillaris), start to die.¹⁰ This damage starts as small spots that grow into larger patches. As the light-sensitive cells in the macula die off, the person starts to lose vision in that eye. At first, the person may notice problems with reading or night vision.⁹ Eventually, the person will develop large, permanent blind spots (scotomata) in the center of the visual field. When the central fovea of the macula is involved, the person loses the ability to have sharp vision, such as that needed for reading and for recognizing faces.⁹

It’s important to note that while GA is commonly associated with people with visual acuity (VA) of 20/200 (or worse) caused by advanced AMD, more than half of all people who develop GA may experience substantial impairment of everyday visual function, which may significantly affect their quality of life.¹¹

The early signs of AMD (drusen and pigmentary changes) are common in individuals over age 65 and precede the late stage forms.¹⁰

While the mechanisms that cause GA are not fully understood, the cause of GA is thought to be multifactorial, with numerous environmental and genetic risk factors. The dysregulation of the complement cascade, an important part of the body’s immune system, may play a pivotal role.⁹

GA is not a hereditary disease. Nevertheless, some genes do increase the risk that a person’s AMD will progress to GA.¹²

GA can be distinguished from other forms of dry AMD by ophthalmic exam and color fundus photography.¹⁰

Spectral-domain optical coherence tomography (SD-OCT) and fundus autofluorescence (FAF) allow for noninvasive and rapid quantitative morphological assessment of GA in the clinical setting.¹⁰

There is no approved treatment to prevent the onset and progression of GA.¹⁰ Several therapeutics are in various stages of clinical development.

The complement system is an integral part of our immune defense system. In healthy people, complement orchestrates the destruction and clearance of pathogens or of the body’s own cells that need to be removed. It also has proinflammatory capabilities.⁸

Complement activation is regulated to avoid its overactivation and to protect the body against inappropriate immune attack. When regulation is compromised, hyperactivation of the complement cascade can lead to inflammation and inappropriate cell destruction.⁸

Three pathways converge with the cleavage of complement factor C3, which induces inflammation and labels cells for phagocytosis (destruction by special white blood cells). The complement cascade continues with the cleavage of complement factor C5, which triggers cell death via phagocytosis, inflammation, and ultimately activation of the membrane attack complex (MAC) which causes damage and cell death.⁸