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Neuroprotective strategies for retinal disease
Open accessAbstract
Diseases that affect the eye, including photoreceptor degeneration, diabetic retinopathy, and glaucoma, affect 11.8 million people in the US, resulting in vision loss and blindness. Loss of sight affects patient quality of life and puts an economic burden both on individuals and the greater healthcare system. Despite the urgent need for treatments, few effective options currently exist in the clinic. Here, we review research on promising neuroprotective strategies that promote neuronal survival with the potential to protect against vision loss and retinal cell death. Due to the large number of neuroprotective strategies, we restricted our review to approaches that we had direct experience with in the laboratory. We focus on drugs that target survival pathways, including bile acids like UDCA and TUDCA, steroid hormones like progesterone, therapies that target retinal dopamine, and neurotrophic factors. In addition, we review rehabilitative methods that increase endogenous repair mechanisms, including exercise and electrical stimulation therapies. For each approach, we provide background on the neuroprotective strategy, including history of use in other diseases; describe potential mechanisms of action; review the body of research performed in the retina thus far, both in animals and in humans; and discuss considerations when translating each treatment to the clinic and to the retina, including which therapies show the most promise for each retinal disease. Despite the high incidence of retinal diseases and the complexity of mechanisms involved, several promising neuroprotective treatments provide hope to prevent blindness. We discuss attractive candidates here with the goal of furthering retinal research in critical areas to rapidly translate neuroprotective strategies into the clinic.
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“Neuroprotective factors that support the survival of retinal cells, such as glial cell-derived neurotrophic factor (GDNF), ciliary neurotrophic factor (CNTF), brain-derived neurotrophic factor (BDNF), basic fibroblast growth factor, and pigment epithelium-derived factor (PEDF) have shown promise in mouse models of retinal degeneration.67,103–105”
From Gene Therapy for Retinal Degenerative Diseases: Progress, Challenges, and Future Directions (2023) · cites this paper as [104]
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Metadata
- Authors
- Pardue, M. T., & Allen, R. S.
- Affiliations
- Georgia Institute of Technology (US)
- Atlanta VA Medical Center (US)
- Corresponding author
- Pardue, Machelle T.
- Venue
- Progress in Retinal and Eye Research
- Publisher
- Elsevier BV
- Published
- 2018-07
- Volume
- 65
- Pages
- 50-76
- ISSN
- 1350-9462 (ISSN-L)
- PMC
- PMC6081194
- OpenAlex
- W2793623156
- Cited by
- 237
- References
- 416
- Citations by year
- 2026: 21 · 2025: 24 · 2024: 30 · 2023: 31 · 2022: 37 · 2021: 37 · 2020: 32 · 2019: 19 · 2018: 5
- FWCI
- 2.28
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Progress in Retinal and Eye Research (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- IRB
- National Institutes of Health (P30 EY006360)
- Rehabilitation R&D Service of the Department of Veterans Affairs (I01RX000951)
- Topics
- Health Sciences › Medicine › Ophthalmology › Retinal Development and Disorders
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Medicine › Ophthalmology › Glaucoma and retinal disorders
- Keywords
- neuroprotection, retinal disease, photoreceptor degeneration, diabetic retinopathy, glaucoma, vision loss, bile acids, ursodeoxycholic acid, tauroursodeoxycholic acid, progesterone, retinal dopamine, neurotrophic factors, exercise therapy, electrical stimulation, retinal cell death, translational therapy
- MeSH terms
- Animals, Electric Stimulation Therapy, Exercise Therapy, Humans, Nerve Growth Factors, Neurons, Retina, Retinal Diseases, Taurochenodeoxycholic Acid, Ursodeoxycholic Acid, Vision Disorders, Cell Death, Neuroprotective Agents
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