What: Inhibiting thyroid hormone (TH) activity helps protect against retinal degeneration in an animal model of AMD.
Where: Ma, H et al, “Inhibition of thyroid hormone signaling protects retinal pigment epithelium and photoreceptors from cell death in a mouse model of age-related macular degeneration.” Cell Death & Disease, 2020
BrightFocus Connection: This project was supported by a Macular Degeneration Research grant to senior author Xi-Qin Ding, PhD, University of Oklahoma Health Sciences Center.
Why It Is Important: Age-related macular degeneration (AMD) has been linked to multiple factors that include aging, chronic inflammation, and genetic defects. Oxidative stress, causing damage to retinal tissue, is recognized to play a major role in AMD.
In addition, recent studies have suggested that high levels of thyroid hormone (TH) may increase risk. To test that hypothesis, the authors investigated what happens when TH levels are suppressed in an oxidative stress-induced animal model of AMD. Their results showed that anti-thyroid treatment protected retinal function and suppressed gene expression associated with cellular stress responses, inflammatory responses, and cell death signaling.
While TH signaling has been linked to other types of neurodegenerative conditions, including Alzheimer’s disease, this work provides some of the first direct evidence that it plays a role in AMD. Additional studies are needed to determine why suppression of TH activity protects against retinal degeneration, and whether that has therapeutic significance for AMD.
About BrightFocus Foundation
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Featured Grant Recipients
Xi-qin Ding, PhD
University of Oklahoma Health Sciences Center