By K. Tsubota
A number of the ailments resulting in blindness comparable to cataract, glaucoma, diabetic retinopathy and age-related macular degeneration correlate with the patient's age. Even genetic problems equivalent to retinitis pigmentosa could be thought of 'premature getting older of the retina', and extra, dry eye or presbyopia, that could dramatically have an effect on caliber of imaginative and prescient, are age comparable. Antiaging learn turns into an increasing number of vital nowadays, even supposing the basics are usually not but common general within the hospital; notwithstanding, reactive oxygen species regulate appears the start. sooner or later, a formal vitamin, together with calorie restrict or antioxidant nutrition elements, antioxidant supplementations, workout in addition to drug intervention may well play an important function within the fight opposed to age-related eye issues. This quantity indicates the newest advancements and may be a beneficial replace with regards to age-related eye ailments not just for ophthalmologists, but in addition for common physicians.
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Extra resources for Anti-aging in Ophthalmology: Special Issue: Ophthalmic Research 2010, Vol. 44, No. 3
34 Kotecha A, Izadi S, Jeffery G: Age-related changes in the thickness of the human lamina cribrosa. Br J Ophthalmol 2006;90:1531– 1534. 35 Hernandez MR, Luo XX, Andrzejewska W: Age-related changes in the extracellular matrix of the human optic nerve head. Am J Ophthalmol 1989; 107:476–484. Ophthalmic Res 2010;44:173–178 177 36 Hernandez MR, et al: Localization of collagen types I and IV mRNAs in human optic nerve head by in situ hybridization. Invest Ophthalmol Vis Sci 1991; 32:2169–2177. 37 Morrison JC, et al: Aging changes of the rhesus monkey optic nerve.
In addition to providing cellular energy via oxidative phosphorylation, mitochondria regulate several key processes such as apoptosis, cell growth, calcium homeostasis and production of reactive oxygen species (ROS). Mitochondria are particularly susceptible to damage due to a close proximity to ROS production and a lack of DNA protection by histones. 175 pathogenesis. Suggested mechanisms include direct cytotoxic effects of ROS on retinal ganglion cells, ROS signaling as a second messenger in retinal ganglion cell apoptosis, ROS-induced glial dysfunction as a cause for secondary retinal ganglion cell death, oxidative damage as an activator of aberrant immune responses or oxidative stress as a trigger for the release of excitotoxic amino acids [50, 51].
MtDNA is particularly vulnerable to oxidative damage, due in part to its close proximity to the inner mitochondrial membrane where the majority of the ROS are generated and the fact that it does not contain histones which are thought to act as a physical barrier against ROS in the nuclear genome . Furthermore it appears that oxidative damage to mtDNA is more extensive and persists longer compared to nDNA damage . Such ROS-induced mtDNA damage includes base modifications, abasic sites, strand breaks and bulky adducts as well as a number of covalent modifications to DNA, which encompass single-nucleobase lesions, strand breaks, inter- and intrastrand cross-links, along with protein-DNA cross-links [78, 79].