Aetiological and immunological aspects of AMD, a leading cause of blindness
in Western countries, have been reviewed. Developmental studies suggest th
at anatomical features unique to the fovea result in a critical relationshi
p between metabolic demand and blood supply at the macula, which is maintai
ned throughout life. Recent studies show a sufficient degree of consistency
in the link between smoking and both dry and wet AMD to regard it as causa
tive. Dry AMD is considered to be the natural endstage of the disease; epid
emiological and morphological studies point to choroidal vascular atrophy a
s the causative event and it is suggested that signals associated with acut
e vascular compromise lead to the development of subretinal neovascularisat
ion. The relationship between sub-pigment epithelial deposits, including ba
sal laminar deposit, and the pathogenesis of AMD is examined, Much of the l
iterature is consistent with a choroidal origin for the constituents of dru
sen. The blood retinal barrier preserves the physiological environment of t
he neural retina and limits inflammatory responses. The factors, including
cytokines, adhesion molecules and the presence of resident immunocompetent
cells (microglia), which determine the immune status of the retina are cons
idered. Historical descriptions of the involvement of inflammatory cells ar
e provided, evidence implicating inflammation in the pathogenesis of AMD in
volving macrophages, giant cells and microglia has been derived from observ
ations of human and animal subretinal neovascular lesions. The role of humo
ral factors such as anti-retinal autoantibodies and acute phase proteins to
gether with clinical observations has been surveyed. Taken together these d
ata demonstrate the involvement of both cellular and humoral immunity in pa
thogenesis of AMD. It remains to be determined to what degree the influence
of immunity is causative or contributory in both wet and dry AMD, however,
the use of anti-inflammatory agents to ameliorate the condition further in
dicates the existence of an inflammatory component, (C) 2001 Elsevier Scien
ce Ltd. All rights reserved.