Understanding the Role of Sleep Apnea Syndrome in AMD

Florian Sennlaub, MD, PhD
Fondation Voir et Entendre (Paris, France)
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July 1, 2018 to June 30, 2020
Macular Degeneration
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Florian Sennlaub, MD, PhD

Influence of Chronic Intermittent Hypoxia on Neuroinflammation in AMD


It has recently been shown that patients with sleep apnea syndrome (SAS) suffer more frequently from age-related macular degeneration (AMD), but the reason for the association of both diseases remains obscure. Our preliminary data suggest that the episodes of hypoxia that characterize sleep apnea activate circulating immune cells and lead to longer and stronger detrimental inflammation in the eye in AMD models. Our project to study immune cell activation and detrimental inflammation by hypoxia might help explain the association of sleep apnea with AMD, and also that of other diseases, such as Alzheimer disease, that are associated with SAS and harmful inflammation. Increased awareness of this mechanism will help to diagnose and treat SAS in affected AMD patients, reducing their need for intra-vitreal injections and slowing the macular degeneration in the future. 


AMD is a multifactorial disease that is due to the unfortunate interaction of genetic risk factors and environmental factors. We have previously shown how a variant of the complement factor H (CFH), which is the strongest inherited risk factor, impedes with the physiological clearance of retinal macrophages and encourages chronic, detrimental inflammation. Sleep apnea syndrome, characterized by episodes of chronic intermittent hypoxia, is very common in the elderly, and has recently been demonstrated to be an important environmental risk factor for debilitating late AMD. The reason for this association is unknown. Our preliminary data suggest that hypoxia that characterize sleep apnea, activates circulating immune cells and lead to increased expression of inflammatory cytokines and CFH that promote longer and stronger detrimental inflammation in the eye in AMD. We will study how experimental sleep apnea induces systemic immune cell activation and detrimental inflammation in the eye. Ultimately this work will improve our understanding of how the interplay of AMD risk factors induce debilitating late AMD, the basis for the development of new efficient therapies.

About the Researcher

Dr. Florian Sennlaub received his medical degree in Germany, his doctoral training and PhD in Paris, and his postdoctoral training in Montréal. He holds a tenure-track director of research position at the French National Health Institute and is head of the Department of Pathophysiology and Therapeutics at the Vision Institute in Paris, France. His laboratory focuses on the pathogenic role of the chronic accumulation of immune cells, in particular macrophages, in age-related macular degeneration (AMD). His recent work has demonstrated how the genetic AMD-risk variants affect macrophage function, impairing subretinal immune suppression, and inflammation resolution. Together his findings emphasize the role of the AMD-risk variants in inflammation in AMD and open new therapeutic avenues to inhibit pathogenic, non-resolving, subretinal macrophage accumulation in AMD. Dr. Sennlaub is the recipient of the Prix de la Fondation de l’oeil (France) and has authored and co-authored 95 articles.

Personal Story

Twenty years ago, during my residency in ophthalmology, I realized how little help there was to offer to patients losing their eyesight due to age related macular degeneration (AMD). The lack of treatment reflected shortcomings in our understanding of the origins of the disease. Since those days, great progress has been made in our ability to treat pathological leaky neo-vessels that destroy vision in many people affected by "wet" AMD, but we are still unable to halt the debilitating, slow neuro-degenerative processes of "wet" and "atrophic" (or “dry”) AMD. The key to understanding the disease process and to developing efficient therapies is to understand more about the environmental and genetic risk factors that trigger the disease in the first place. Work from our laboratory and others has helped us to appreciate how genetic variants lay the groundwork for detrimental chronic inflammation in the disease process. Thanks to this BrightFocus grant, we will understand to what degree sleep apnea, an increasingly recognized risk factor of AMD, further fuels the chronic inflammation that induces retinal degeneration. Increased awareness of this mechanism will help us to diagnose and treat sleep apnea in affected AMD patients, inhibiting inflammation, degeneration and vision loss in the future. This project would not have been possible without the support of BrightFocus and its donors. Thank you.

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