AMD is an eye disease whose onset is related to a variety of risk factors, first and foremost the physiological ageing process.
Other risk factors include DMLE, https://www.oculistaitaliano.it/articoli/ruolo-dellinfiammazione-nelle-patogenesi-della-degenerazione-maculare-legata-alleta/), blue light, the electromagnetic radiation of the visible spectrum between 380 and 500 nm, has also been identified. Blue light is, among other things, emitted by all PC, smartphone, tablet and TV screens, as well as by LED lights; in essence, therefore, by most light sources to which our eyes are exposed on a daily basis.
AMD is a progressive degenerative disease that, if not adequately treated, can lead to the loss of central vision.
There are two types of AWD: i) the dry form and (ii)the wet one (or neovascular).
The dry form characterises approximately 90% of all macular degeneration and is caused by the accumulation below the macula of deposits of yellowish material, the drusen, which progressively alter the function of the photoreceptors, cells specialised in vision, and the retinal pigment epithelium (RPE, retinal pigment epithelium).
Wet or exudative AMD, which is fortunately less frequent than dry AMD (approximately 10% of cases), is characterised by an abnormal growth of blood vessels within the retinal region. These vessels, with very fragile walls, can easily ooze fluid, or they can rupture, causing haemorrhages in the retina. The alteration in the growth process of neovases in wet AMD is favoured by a specific factor, the vascular endothelial growth factor (VEGF).
For the prevention and reduction of the risk of the occurrence of this eye disease, the scientific community is trying to identify the molecular mechanisms capable of regulating the production of VEFG and, recently, a step forward in this direction was made by a team of researchers from the Sorbonne University in Paris, France, in collaboration with the University of Pittsburgh, USA.
In particular, the research sought to analyse the effect that blue light has on the expression and secretion of the VEGF factor in retinal pigment epithelium cells 'loaded' with a specific molecule, the A2E molecule. The latter is one of the retinoid lipofuscin compounds that increases VEGF expression and is accumulated in large quantities precisely as a result of the onset of age-related macular degeneration. The results of this study showed that the photosensitiser molecule AE2 was able to induce increased VEGF expression through the activation of retinoid receptors and, in turn, the accumulation in AE2 levels caused stress and oxidative damage to epithelium cells, leading to cell death of the cells. However, the researchers showed that RPE cells loaded with AE2 and exposed to blue light under moderate irradiation for about 15 hours not only reduced VEGF synthesis, but at the same time increased the synthesis of another factor, VEGFR1, which acted by 'trapping' VEGF, thus acting as a protective factor against oxidative stress.
These data therefore suggest that therapy with anti-VEFG substanceswhich to date is one of the main treatment modalities for wet AMD to suppress the growth of neovases, is not only suitable for the resolution of vascular complications, but can also be helpful in limiting damage induced by exposure to blue light.
Source:
M.Marie et al. Blue-violet light decreases VEGFa production in an in vitro model of AMD. PLoS One. 2019; 14(10): e0223839.
Dr. Carmelo Chines
Direttore responsabile
English 
Italian