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Reviews of information about AMD, cataract, and glaucoma make it apparent that while each eye tissue has its own characteristic metabolism, structure, and function, there are common perturbations to homeostasis that are associated with age-related dysfunction. The commonalities appeared to be biochemical stresses and their sequelae. Recognition of shared etiologic factors for age-related debilities allows rationalization of comparable risk factor-disease incidence relationships—such as nutritional risk factors for AMD and cataract (as well as cardiovascular disease and diabetes)—and informs about potential new therapeutic avenues, such as stress reducers (i.e., antioxidants) and/or proteolysis enhancers. It also maximizes the return on the investment in research effort and costs. For example, drugs or nutrients that protect against AMD may also prove effective against cataract, glaucoma, or/and other age-related neurodegenerative debilities.  This article summarizes cell biologic and biochemical changes in aging and age-related diseases of the eye. Clearly, this is a larger challenge with a richer literature than can be properly treated in a short review such as this. In this short review, we focus on age-related stresses and current and anticipated means to diminish the stress. Recognizing that almost all age-related diseases such as Alzheimer and Parkinson diseases, cataract, AMD, glaucoma, diabetes, and the premature aging diseases such as progeria, have in common the accumulation of damaged proteins, we select three aspects of age-related biochemical changes that are common to most eye tissues: oxidative stresses; problems associated with and/or due to damaged proteins that accumulate in the retina, lens, and cornea; and intracellular degradative capacities that usually keep levels of damaged proteins in check in early life or when tissues are not stressed, but that may fail upon stress or aging (Figs. 1, ​,2).2). We offer apologies to investigators whose work we do not cite or can acknowledge only via reviews.1    Figure 1  Scheme of proposed relationship between chronic stress, protective capacities, proteolytic editing machinery and age-related disease. When young, proteins are intact and cell and tissue functions are retained. Upon exposure to various stresses (red) including ...Figure 2  Upon aging, proteins are damaged. This damage includes various modifications such as oxidations, reaction with other moieties such as sugar derivatives, cross linking (yellow), and lysis. These processes accelerate upon aging (follow blue line) and parallel ...    The most rapidly growing segment of many societies is the elderly. The prevalence of cataract, AMD, and glaucoma accelerates with age. Among those who are aged 75 years or older, prevalence rates of cataract, AMD, and glaucoma are approximately 60%, 15%, and 20% of the population, respectively. These estimates almost double for people aged just 10 years older. Like most tissues in general, most eye tissues suffer from the accumulation of damaged proteins. Such accumulation appears to involve post-synthetic modifications to proteins and limits on the proteolytic capacities that are normally available to degrade and remove the altered or obsolete proteins before they transform into cytotoxic aggregates. Collectively, we call the sum of synthesis, post-synthetic modification, editing and removal of proteins “proteopoise.” Compromises to proteopoise are also thought to be etiologic for many age-related neuropathies and premature aging syndromes.1–7 Herein, we work our way from the anterior of the eye, or cornea, through to the lens and on to the posterior segment or retina, recalling common themes of age-related changes and protein quality control.

investigative ophthalmology and visual science

Common Cell Biologic and Biochemical Changes in Aging and Age-Related Diseases of the Eye: Toward New Therapeutic Approaches to Age-Related Ocular Diseases