The changes in the RPE-Bruch's membrane complex contribute to the death of multiple retinal neurons, this translating as a thinning and disorganization of its layers.Cholesterol is essential for cell functioning. The main cholesterol source for the photoreceptors and the RPE comes from extracellular lipid metabolism, as has been demonstrated on detecting native low-density lipoprotein (LDL) receptors at the RPE level [12], which could be involved in the local production of apolipoprotein E (apoE). The retina also locally produces lipoprotein particles that contain apoE. These particles are secreted fundamentally by the Müller glia to the extracellular retinal compartment and to the vitreous, from which they are transported to the optic nerve [13]. Also, the retinal astrocytes associated with the axons of the ganglion cells participate in the secretion of apoE. This cholesterol transport is essential to supply the retinal neurons the lipids needed for the maintenance and remodelling of their cell membrane.
PurposeTo quantify different morphological signs of microglial cells activation, as well as to analyze the P2RY12, MHC‐II and CD68 expression in 15‐month old mice , an early stage of aging (aged naïve) in comparison with a young adult mice (young naïve).MethodsYoung naïve (n = 6) and aged naïve (n = 6) mice were analyzed. Retinal whole‐mounts were immunolabeled with: 1) anti Iba‐1 to quantify: i) Iba‐1 + cells number (Ibacn) in outer segments (OS), outer plexiform layer (OPL) and inner plexiform layer (IPL); ii) area of retina occupied by Iba‐1 + cells (Iba‐1 RA) in the nerve fiber layer‐ ganglion cell layer (NFL‐GCL) iii) cell body area of Iba‐1+ cells (CbIbac) in OPL, IPL and NFL‐GCL; iv) arbor area of Iba‐1+ cells (AAIbac) in OPL and IPL; number of vertical processes of Iba‐1+ cells (VPIbac) beetween the OS and OPL. 2) anti‐P2RY12 to identify resident microglia, anti‐CD68 and anti‐MHC‐II as a microglial activation marker.ResultsIn aged naïve with respect to young naïve the quantitative analysis showed: i) a non‐significant increase in the Ibacn in OS; ii) a non‐significant decrease in the AAIbac in OPL; iii) a significant increase in the CbIbac in OPL, IPL and NFL‐GCL and iv) a significant increase in the VPIbac. When we analyzed the expression of P2RY12, CD68 and MHC‐II we observed: i) in young naïve all Iba‐1+ cells were P2RY12+, except perivascular and dendritic cells, but in the aged naïve some cells were Iba‐1+/P2RY12‐; ii) in aged naïve numerous amoeboid‐like CD68+ cells were found while in the young naïve the expression of CD68 practically was absent, and iii) in both young naïve and aged naïve no expression of MHC‐II was observed.ConclusionsIn 15‐month‐old mice, morphological changes and in the expression of P2RY12, CD68 and MHC‐II occurs in the microglial cells compared to young adult mice. These signs show a non‐pathological state of microglial activation that could influence of retinal age‐related disorders.
PurposeAlzheimer’s diseases is a neurodegenerative disease, whose signs can appear decades before clinically detectable symptoms. In addition to age, genetic factors are one of the most important risk factors. The aim of the present study was analyzed the macular thickness changes by optical coherence tomography (OCT) in subjects who have a first‐degree family history of AD and are carriers of ɛ4 allele for the ApoE, which are two of the main risk factors for developing the disease.MethodsA complete eye examination and a macular OCT were performed in 64 participants, who were free of ocular pathology. The two study groups were formed by 35 subjects with a family history of AD (FH+) and ApoE ɛ4 carriers and 29 age‐matched control subjects without a family history of AD (FH‐) and ApoE ɛ4 non‐carriers.ResultsWe found a statistical significant thinning (p < 0.05) in FH+ ApoE ɛ4 carriers compared to FH‐ ApoE ɛ4 non‐carriers in the next sectors and layers: the foveal area of the macular retinal nerve fiber layer (11.89 ± 1.95, FH+ vs 12.86 ± 1.62, FH‐); the inferior and nasal sectors, both in the outer (26.77 ± 2.74, FH+ vs 28.17 ± 2.82, FH‐) (29.49 ± 2.89, FH+ vs 30.93 ± 3.85, FH‐) and inner (40.49 ± 2.51, FH+ vs 42.10 ± 3.48, FH‐) (41.94 ± 2.74, FH+ vs 43.52 ± 3.57, FH‐) macular ring in the inner plexiform layer; the foveal area (18.82 ± 3.61, FH+ vs 21.21 ± 3.88, FH‐) and the inferior sector in the outer macular ring (30.91 ± 2.72, FH+ vs 32.10 ± 2.81, FH‐) in inner nuclear layer, and the inferior sector of the outer macular ring (27.60 ± 2.75, FH+ vs 29.97 ± 3.82, FH‐) in outer plexiform layer.ConclusionsThe slight retinal thickness changes measured by OCT, that appear in the macular area in asymptomatic subjects at high genetic risk for the development of AD, could be used as an early biomarker of the disease.
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