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      Age-Related Macular Degeneration: Insights into Inflammatory Genes

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          Abstract

          Age-related macular degeneration (AMD) is a progressive neurodegenerative disease that affects approximately 8.7% of elderly people worldwide (>55 years old). AMD is characterized by a multifactorial aetiology that involves several genetic and environmental risk factors (genes, ageing, smoking, family history, dietary habits, oxidative stress, and hypertension). In particular, ageing and cigarette smoking (including oxidative compounds and reactive oxygen species) have been shown to significantly increase susceptibility to the disease. Furthermore, different genes ( CFH, CFI, C2, C3, IL-6, IL-8, and ARMS2) that play a crucial role in the inflammatory pathway have been associated with AMD risk. Several genetic and molecular studies have indicated the participation of inflammatory molecules (cytokines and chemokines), immune cells (macrophages), and complement proteins in the development and progression of the disease. Taking into consideration the genetic and molecular background, this review highlights the genetic role of inflammatory genes involved in AMD pathogenesis and progression.

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          Innate immunity.

          R Medzhitov, C A Janeway (2000)
          Article 0 comments Cited 398 times – based on 0 reviews     Review now
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            The NLRP3 inflammasome: a sensor for metabolic danger?

            Kate Schroder, Rongbin Zhou, Jurg Tschopp (2010)
            Interleukin-1beta (IL-1beta), reactive oxygen species (ROS), and thioredoxin-interacting protein (TXNIP) are all implicated in the pathogenesis of type 2 diabetes mellitus (T2DM). Here we review mechanisms directing IL-1beta production and its pathogenic role in islet dysfunction during chronic hyperglycemia. In doing so, we integrate previously disparate disease-driving mechanisms for IL-1beta, ROS, and TXNIP in T2DM into one unifying model in which the NLRP3 inflammasome plays a central role. The NLRP3 inflammasome also drives IL-1beta maturation and secretion in another disease of metabolic dysregulation, gout. Thus, we propose that the NLRP3 inflammasome contributes to the pathogenesis of T2DM and gout by functioning as a sensor for metabolic stress.
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              A role for local inflammation in the formation of drusen in the aging eye.

              Don H Anderson, Robert F. Mullins, Gregory Hageman … (2002)
              The accumulation of numerous or confluent drusen, especially in the macula, is a significant risk factor for the development of age-related macular degeneration (AMD). Identifying the origin and molecular composition of these deposits, therefore, has been an important, yet elusive, objective for many decades. Recently, a more complete profile of the molecular composition of drusen has emerged. In this focused review, we discuss these new findings and their implications for the pathogenic events that give rise to drusen and AMD. Tissue specimens from one or both eyes of more than 400 human donors were examined by light, confocal or electron microscopy, in conjunction with antibodies to specific drusen-associated proteins, to help characterize the transitional events in drusen biogenesis. Quantification of messenger RNA from the retinal pigment epithelium (RPE)/choroid of donor eyes was used to determine if local ocular sources for drusen-associated molecules exist. The results indicate that cellular remnants and debris derived from degenerate RPE cells become sequestered between the RPE basal lamina and Bruch's membrane. We propose that this cellular debris constitutes a chronic inflammatory stimulus, and a potential "nucleation" site for drusen formation. The entrapped cellular debris then becomes the target of encapsulation by a variety of inflammatory mediators, some of which are contributed by the RPE and, perhaps, other local cell types; and some of which are extravasated from the choroidal circulation. The results support a role for local inflammation in drusen biogenesis, and suggest that it is analogous to the process that occurs in other age-related diseases, such as Alzheimer's disease and atherosclerosis, where accumulation of extracellular plaques and deposits elicits a local chronic inflammatory response that exacerbates the effects of primary pathogenic stimuli.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Ophthalmol
                Journal ID (iso-abbrev): J Ophthalmol
                Journal ID (publisher-id): JOPH
                Title: Journal of Ophthalmology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-004X
                ISSN (Electronic): 2090-0058
                Publication date (Print): 2014
                Publication date (Electronic): 12 November 2014
                Volume: 2014
                Electronic Location Identifier: 582842
                Affiliations
                1Department of Biomedicine and Prevention, School of Medicine, University of Rome “Tor Vergata”, Via Montpellier 1, 00133 Rome, Italy
                2UOSD Retinal Pathology PTV Foundation “Policlinico Tor Vergata”, Viale Oxford 81, 00133 Rome, Italy
                3Molecular Genetics Laboratory UILDM, Santa Lucia Foundation, Via Ardeatina 354, 00142 Rome, Italy
                Author notes

                Academic Editor: Haoyu Chen

                Author information
                http://orcid.org/0000-0002-2148-0758
                http://orcid.org/0000-0003-1334-0920
                Article
                DOI: 10.1155/2014/582842
                PMC ID: 4247975
                PubMed ID: 25478207
                SO-VID: 8711d419-b7c4-4db3-b450-dbb8d3470cde
                Copyright © Copyright © 2014 Raffaella Cascella et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 31 July 2014
                Date revision received : 23 October 2014
                Date accepted : 23 October 2014
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Ophthalmology & Optometry
                Data availability:
                ScienceOpen disciplines: Ophthalmology & Optometry

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