A glimpse at the aging eye

Abstract

Extensive investigations have demonstrated that organismal aging is associated with tissue dysfunction in many organs. The eye is no exception to this rule. Under healthy conditions, the eye is designed like an advanced camera with the central role of translating light from the external world into a coherent neural signal that can be transmitted to the brain for processing into a precise visual image. This complex process requires precisely maintained machinery. At the front of the eye, the transparency of both the cornea and the lens are crucial to allow passage of photons to the light-sensitive portion of the eye. Similarly, the highly organized structure of the retina located at the back of the eye is indispensable to allow for effective signal transduction and efficient signal transmission. Aging affects ocular structures in various ways, and these sequelae have been well defined as distinct clinical entities. In many instances, aging leads to ocular tissue dysfunction and disease. Nonetheless, despite clear evidence that age-associated visual impairment has significant psychosocial consequences, current treatment paradigms for many of these conditions are inadequate. In addition, strategies to decelerate or reverse age-associated deterioration in ocular function are still in their infancy. This review focuses on the cellular and molecular pathophysiology of the aging eye. Ultimately, we hope that a refined understanding of the aging eye can guide targeted therapies against cellular aging and disease.

Figure 1

Glutaraldehyde-/formalin-fixed mouse retina stained with hematoxylin and eosin (HE) depicting the layers of the retina and other ocular structures: lens, inner limiting membrane (ILM), nerve fiber layer (NFL), ganglion cell layer (GCL), inner plexiform layer (IPL), inner nuclear layer (INL), outer plexiform layer (OPL), outer nuclear layer (ONL), external limiting membrane (ELM), inner segments (IS) & outer segments (OS) of the photoreceptors, retinal pigment epithelium (RPE), choroid and optic nerve.

Figure 2

Major age-associated ocular diseases and the structures that they affect.

Figure 3

Fundoscopic images from AMD patients demonstrating hallmarks of disease, such as drusen (a; examples indicated by arrows), geographic atrophy (b; roughly outlined by dashed white line) and choroidal neovascularization (c; roughly outlined by dashed white line).

Figure 4

Fundoscopic image from a healthy patient with a small cup-to-disc ratio and a healthy, pink optic disc surrounding the cup (a) compared with a fundoscopic image from a severely glaucomatous patient with an enlarged cup and significant inferior thinning of the disc rim (b). Dashed white circles roughly outline the cups; solid white circles roughly outline the discs.

Figure 5

Slit-lamp photograph of a patient with severe dry eye syndrome whose ocular surface was stained with fluorescein. Note the abnormal staining on the corneal epithelium (see arrows).