We present the following article in accordance with the STROBE reporting checklist (available at ). The aim of the present study is to provide visualization of the evolution of various tomographic intraretinal layer thicknesses during aging and to document age-related changes in focal thickness. However, no studies have provided visualization of the evolution of various tomographic intraretinal layer thicknesses during aging. Only one study provided visualization of the tomographic thickness pattern of GCIPL averaged from a group of healthy subjects, and it demonstrated thinner GCIPL in the inferior sector ( 10). The majority of the studies differentiated sectorial thinning by commonly used partitions including the early treatment of diabetic retinopathy study (ETDRS) ( 8) and Zeiss elliptical partition ( 6, 7). Also, previous studies showed uneven alterations (sectorial thinning) of the GCIPL due to aging ( 6- 10). Based on the average thickness of the neuronal layers, including RNFL and GCIPL, previous studies have documented that age plays a role in retinal neurodegeneration ( 6- 8, 10). Retinal neurodegeneration during aging, such as the reduction in thickness of the retinal nerve fiber layer (RNFL) and ganglion cell-inner plexiform layer (GCIPL) measured by optical coherence tomography (OCT), has been reported ( 3- 10). It provides an opportunity to study both physiological and pathophysiological mechanisms related to aging ( 3, 4). The retina is an extension of the brain and provides a unique opportunity for studying the effect of aging on the central nervous system. Morphological alterations, such as axonal swelling, microtubule disassembly, and nerve cell body loss, are characteristic features in many neurodegenerative conditions ( 2). Receptor dysfunctions may be implicated in morphological and functional impairments of retinal inner layer formation associated with eye disorders.Neurodegeneration is an age-associated progressive deterioration of neuronal structures and functions, which may lead to cognitive impairment and affect lifespan potentials ( 1). Altogether, these data suggest a novel role of SORLA in synaptogenesis. In line with receptor expression in dendritic terminals, we found delayed stratification of the inner plexiform layer in knockout mice, indicating an involvement of SORLA in neuronal connectivity. Interestingly, we found that transcripts are somatically located in several neuronal populations residing in the INL and the ganglion cell layer, whereas SORLA protein is also present in the synaptic plexiform layers. qPCR and Western blot analyses showed that SORL1/SORLA expression peaks at postnatal day 15, just after eye opening. Using stereological analysis, we confirmed previous studies showing that receptor depletion in knockout mice significantly reduces the number of cells in the inner nuclear layer (INL), suggesting that functional SORLA expression is essential for the development of this retinal strata. Here, we provide a spatio-temporal characterization of SORL1 mRNA and its translational product SORLA in the postnatal mouse retina. Recently, involvement of SORLA in retinogenesis was proposed, but no studies have examined yet in detail the expression pattern of this sorting receptor in the retina. Sorting protein-related receptor containing LDLR class A repeats (SORLA also known as LR11) exerts intraneuronal trafficking functions in the central nervous system.

Plexiform layers