Abstract
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.
Highlights
Since Ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid (TUDCA) target apoptosis and endoplasmic reticulum (ER) stress, perhaps these results suggest that these pathophysiological mechanisms affect the retinal neurons regardless of the origin of the disease or the endstage manifestations
Reduced dendritic branching and synaptic contacts with AII amacrine cells has been observed in dopaminergic amacrine cells in several models of retinal degeneration, indicating that dopamine may play a role in functional loss in these diseases as well (Ivanova et al, 2016)
A simple piercing wound through the eye ball causes the upregulation of basic fibroblast growth factor (FGF 2), brain derived neurotrophic factor (BDNF) and ciliary neurotrophic factor (CNTF) in a localized region which will protect the retina from degeneration due to light damage (Wen et al, 1995) or hereditary retinal disease (Faktorovich et al, 1990)
Summary
We are focused on neuroprotective interventions that slow vision loss caused by retinal disease. Reduced visual acuity and blindness is associated with diminished quality of life measures due to limited social interactions and independence, loss of employment, and depression (Coffey et al, 2014; Cumberland and Rahi, 2016; Khorrami-Nejad et al, 2016; Papadopoulos et al, 2013; Senra et al, 2013). This is especially true for retinal diseases that compromise the macular region, thereby affecting the ability to read and recognize faces (Taylor et al, 2016). Successful neuroprotective strategies could provide months or years of useful vision that would allow an individual to continue to be gainfully employed and maintain their independence and quality of life
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