Because ARMS2 is an evolutionarily recent primate-specific gene and because the ARMS2 / HTRA1 genetics are found at a locus on chromosome 10q26 in an area with strong linkage disequilibrium [ 14 ], whether ARMS2 is the key gene leading to AMD is debatable.

Before we evaluate the relationships between

ARMS2

polymorphisms and ADVANCED MICRO DEVICES, we must summarize the basic information available about

ARMS2

polymorphisms (Table 

1

). Recently, Grassmann et al. [

15

] demonstrated that genetic variants in or near to

ARMS2

but not

HTRA1

are responsible for disease susceptibility at the 10q26 locus. These results encourage a concentrate on functional analyses of

ARMS2

and its role within AMD pathogenesis [

15

], even though a study by Yg et al. [

16

] suggested that a version of the

HTRA1

gene increased susceptibility to ADVANCED MICRO DEVICES. Jabbarpoor Bonyadi et al. considered that

ARMS2

/LOC387715 and

CFH

share a common pathway, possibly the enhance system pathway, in AMD pathogenesis, and proposed these genes might have a synergistic effect in AMD [

17

]. Furthermore,

R38X

,

A69S

, and

R3H

(rs10490923), which are the three common coding variants in the

ARMS2

gene, were tested in a large case-control data established; the analysis showed that the

A69S

variant had been significantly associated with AMD risk. The effect of the

R3H

variant was the opposite after adjustment for sex plus age. Wang et al. [

18

] demonstrated that if the effect of

A69S

is removed, the particular inverse effect of

R3H

is no longer statistically significant, uncovering the strong linkage disequilibrium in this region and showing the fact that

A69S

variant is a strong risk factor just for AMD. Kortvely et al. [

19

] discovered chimeric transcripts of the

PLEKHA1

(pleckstrin homology domain-containing protein family A member 1) gene that ended within

ARMS2

, which may explain how variants in this locus have an effect on AMD. From these studies, it may be concluded that a close relationship in between

ARMS2

variations and AMD exists, but the particular mechanism remains to be confirmed.

Table 1

Basic information for single nucleotide polymorphisms associated with four susceptibility loci in ARMS2

rs10490923

10: 122454735

Intron variant, missense

A/G

A

zero. 022

rs10490924

10: 122454932

Intron variant, missense

G/T

T

0. 402

rs2736911

10: 122454839

Intron variant, stop gained

C/T

T

0. 122

rs2736912

10: 122456078

Intron variant

C/T

T

0. 081