**2. Epidemiology, risk factors, and natural history**

#### **Prevalence and incidence**

In last 30 years were published many epidemiological studies on AMD. In a meta-analysis of population-based studies in white people aged 40 years and older, the prevalence of early

age-related macular degeneration was estimated to be 6.8% and late age-related macular de‐ generation 1.5%[3].

C2, CFB, C3 and CFI.29-31. On the basis of large genome-wide association studies, HDL cho‐ lesterol pathway genes have been implicated, including LIPC and CETP, and possibly AB‐ CA1 and LPL.32-34 APOE in the LDL pathway might also be related to AMD [13]. The collagen matrix pathway genes COL10A1 and COL8A1 and the extracellular matrix path‐ way gene TIMP3 have also been linked to age-related macular degeneration [14]. Finally, genes in the angiogenesis pathway (VEGFA) have also been associated with age-related macular degeneration in a meta-analysis of two AMD genome-wide association studies [14].

Classification and Clinical Features of AMD http://dx.doi.org/10.5772/53762 107

Genes modifying several biological pathways are in AMD. Complement and immune proc‐ esses, HDL cholesterol, and mechanisms involving collagen, extra-cellular matrix, and an‐ giogenesis pathways are associated with the onset, progression, and bilateral involvement of AMD [2]. But it should be noted that genetic susceptibility can be modified by environmen‐ tal factors. Genetic variations can also influence differential responses to treatments for age-

Aging is a physiological process involving all body organs and tissues. This process also af‐ fects the eye. It is a physiological process. That is not a manifestation of any disease. Each body cell has a planned life cycle from its inception to apoptosis (cell death). Body tissue in which there is no restoration of extinct mitotic cells (nerve tissue, retina), have a high inci‐

Clinical manifestation of retinal aging is mainly visible as a foveal reflex loss. Its background is in the loss of cells from the inner retinal layers around the foveola and extending of foveal avascular zone [15]. In macular zone are usually present small hard drusen, which are not yet a manifestation of AMD [16]. In macula also occur tigers like irregularities in pigmenta‐ tion. Visual acuity remains on a physiological level unlike of subjects affected by AMD. Doppler velocimetry demonstrates decrease of blood flow to the macular area [17]. Further is detectable reduction of perifoveolar arterioles and venules together with enlargement of

Older age, female sex Cigarette smoking

Obesity, Hypertension, Diabetes mellitus

**Table 1.** Risk factors for age-related macular degeneration (adapted from [2])

related macular degeneration, an emerging research area [2].

Low dietary intake of vitamins A, C, and E, and zinc Low dietary intake of lutein and omega-3 fatty acids Unhealthy lifestyle related to cardiovascular risk factors

Table 2 summarizes major genes associated with onset and progression of AMD

**5. Clinical manifestations of the process of natural retinal aging**

dence of manifestations of aging especially after the 75th year of life.

foveal avascular zone [18] and reduction of retinal ganglion cells amount [19].

Results from the Baltimore Eye Study reported epidemiological data from other ethnic groups. Late AMD was nine to ten times more prevalent in white participants than in black ones [4]. Age-specific prevalence of late age-related macular degeneration in Asians is large‐ ly similar to that in white people [5].

In Asia population have often disease specific features. Many of them have polypoidal dila‐ tation of the choroidal vasculature. Polypoidal choroidal vasculopathy can account for 50% of wet AMD cases in Asians, but only 8-13% in white people [5].

Another variant of AMD is retinal angiomatous proliferation (RAP), which accounts for 12-15% of neovascular age-related macular degeneration [6]. RAP usually not responds to standard management of wet AMD.

There are few incidence studies on AMD. The US Beaver Dam Eye Study in the USA report‐ ed a 14.3% 15-year cumulative incidence for early AMD and 3.1% for late AMD in adults aged 43-86 years [7].
