By D. Virgil Alfaro III et al.
- Learn from a well known team of retina surgeons who deal with all elements of administration, together with anatomy, body structure, and pathophysiology; imaging of the macula in ARMD, prevention measures and remedy; and destiny instructions within the field.
- Gain an effective beginning in intravenous fluorescein angiography, indocyanine eco-friendly angiography, and optical coherence tomography, in addition to antiVEGE remedy and comparable new medicines, optimizing your prognosis and remedy options.
- Understand the numerous switch within the type approach of choroidal neovascular membranes in ARMD.
- Get up to date info on treating ARMD secondary to geographic atrophy via cellphone transplantation and pharmacologic therapies.
- Easily visualize key facets of ARMD due to top of the range illustrations and photographs.
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Additional info for Age-Related Macular Degeneration
Finally, the naturally occurring mouse models include retinal degeneration models with mice exposed to nocive and AMD-related conditions and the senescence-accelerated mouse (SAM) models with systemic and retinal age-related pathology, including BM thickening, basal deposits, and CNV. In the following paragraphs, we explain the most important models of each of the groups mentioned above. Overall, these models contrast with the murine models of wet AMD that are mostly induced mechanically and are explained later in this chapter.
As a result, it was necessary to create mice with combined deficiencies in Cp and Heph so as to assess the potential influence of iron overload in AMD (91). By 5 months of age, these double knockout models had fruitfully increased iron levels and displayed subsequent iron-laden electrondense vesicles inside the RPE cells. Focal areas of RPE hypertrophy and hypopigmentation in the midperipheral retina, subretinal deposits, photoreceptor atrophy, and subretinal neovascularization start appearing at the age of 6 to 9 months, and after a year, these models showed infiltration of macrophages, focal areas of hyperautofluorescence, and complement disposition (92).
In the following paragraphs, we explain the most important models of each of the groups mentioned above. Overall, these models contrast with the murine models of wet AMD that are mostly induced mechanically and are explained later in this chapter. LIPID AND GLUCOSE METABOLISM MODELS A growing body of the literature indicates the involvement of lipids, lipoproteins, and glucose in the formation of extracellular lesions in aging BM, basal deposits and drusen, and other AMD hallmarks. Observational studies have indicated that maintaining adequate levels of fatty acids or a low glycemic index (GI) diet may be particularly beneficial for early stages of the disease.