The aging of the retina
Abstract
This mini-review summarizes our current knowledge concerning the age-related changes that affect the retina. Over the last 10 years, our understanding of the genetics of hereditary retinal diseases has improved considerably. However, the modifications that occur in the retina as a result of aging are still under investigation. In this review, we place particular emphasis on the normal retinal alterations that occur with aging (gene modulation; psychophysical, structural and cellular alterations). We describe the events that occur during the pathological aging process, such as in age-related macular degeneration. Understanding these different modifications is essential if we are to find key players on which to base therapeutic interventions that may help to prevent the passage of normal aging process to the pathological aging process.
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In humans, advanced age is accompanied by increased vulnerability to disease, with progressive and generally irreversible loss of physiological functions; in the eye, these include deficits in visual processing and degenerative changes in retinal neurons and the RPE.
“In humans, advanced age is accompanied by increased vulnerability to disease, with progressive and generally irreversible loss of physiological functions; in the eye, these include deficits in visual processing and degenerative changes in retinal neurons (particularly rods and ganglion cells) and the RPE (16, 78).”
From Unraveling a Multifactorial Late-Onset Disease: From Genetic Susceptibility to Disease Mechanisms for Age-Related Macular Degeneration (2009) · cites this paper as [16]
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“exposed to light and oxidative damage, leading to cellular and molecular alterations such as mitochondrial DNA damage, impaired lysosomal and mitochondrial functions, accumulation of lipofuscin in RPE (Bonnel et al., 2003), local chronic inflammation, and drusen accumulation in the Bruch’s membrane (Booij, Baas, Beise…”
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“As we previously mentioned, the RPE undergoes degenerative changes, Bruch’s membrane thickens with lipid and proteinaceous deposits, 87–89 and cellular waste products such as lipofuscin accumulate, 90 all of which compromise the structural integrity and reparative capacity of the retina.”
- Authors
- Bonnel, S., Mohand-Said, S., & Sahel, J.-A.
- Affiliations
- Centre hospitalier national d'ophtalmologie des Quinze-Vingts (FR)
- Inserm (FR)
- Corresponding author
- Sahel, José-Alain
- ORCID
- Sahel, José-Alain
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2003-08
- Volume
- 38
- Issue
- 8
- Pages
- 825-831
- ISSN
- 0531-5565 (ISSN-L)
- OpenAlex
- W2051373032
- Cited by
- 89
- References
- 91
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 5 · 2023: 4 · 2022: 3 · 2021: 8 · 2020: 4 · 2019: 6 · 2018: 6 · 2017: 4 · 2016: 1 · 2015: 6 · 2014: 5 · 2013: 3 · 2012: 2
- FWCI
- 1.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Gerontology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Retinal Imaging and Analysis
- Keywords
- retinal aging, age-related macular degeneration, inherited retinal disease, gene expression modulation, pathological aging, therapeutic interventions
- MeSH terms
- Aged, Aging, Humans, Macular Degeneration, Psychophysics, Retina, Retinal Diseases, Vision, Ocular, Angiogenesis Modulating Agents
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