PMC:7523471 / 50263-51769 JSONTXT

{"project":"TEST0","denotations":[{"id":"33041751-217-225-816586","span":{"begin":362,"end":366},"obj":"[\"28814675\"]"},{"id":"33041751-121-129-816589","span":{"begin":1263,"end":1267},"obj":"[\"12699953\"]"},{"id":"33041751-140-148-816590","span":{"begin":1282,"end":1286},"obj":"[\"24688166\"]"},{"id":"33041751-234-242-816591","span":{"begin":1478,"end":1482},"obj":"[\"24398104\"]"}],"text":"These findings were corroborated in another study, which indicated a substantial loss of retinal cells at sites of Aβ deposition (Figures 5A–D). When compared with age-matched cognitively normal controls, 22-29% retinal neuronal degeneration was detected by Nissl staining (n = 17 subjects) in the GCL, INL, and ONL of AD patients (Figures 5B,C; Koronyo et al., 2017). More recently, Asanad and colleagues analyzed retinal atrophy morphometrically in the superior quadrants of postmortem retinas from 8 AD and 11 age-matched controls (Asanad et al., 2019b). Measurements were acquired along a distance of 4mm from the optic nerve on the supero-temporal (reaching the macular region) and supero-nasal sides. Significant retinal thinning was revealed in the NFL (∼40%), GCL (35%), IPL (∼20%), and both nuclear layers (25%) in AD patients. In the supero-temporal region, NFL thinning was more pronounced closer to the optic nerve, whereas the other retinal layers showed prominent thinning closer to the macula. However, all analyzed retinal layers showed consistent thinning throughout the supero-nasal retinal quadrant (Asanad et al., 2019b). Beyond these changes, several studies have demonstrated accumulation of Aβ in the lens of AD patients (Goldstein et al., 2003; Tian et al., 2014) as well as reductions in the choroid coat – the vascular layer of the eye – and offered insights into the retinal choroid as an oculovascular biomarker for Alzheimer’s disease (Tsai et al., 2014; Asanad et al., 2019a)."}

{"project":"2_test","denotations":[{"id":"33041751-28814675-38666372","span":{"begin":362,"end":366},"obj":"28814675"},{"id":"33041751-12699953-38666375","span":{"begin":1263,"end":1267},"obj":"12699953"},{"id":"33041751-24688166-38666376","span":{"begin":1282,"end":1286},"obj":"24688166"},{"id":"33041751-24398104-38666377","span":{"begin":1478,"end":1482},"obj":"24398104"}],"text":"These findings were corroborated in another study, which indicated a substantial loss of retinal cells at sites of Aβ deposition (Figures 5A–D). When compared with age-matched cognitively normal controls, 22-29% retinal neuronal degeneration was detected by Nissl staining (n = 17 subjects) in the GCL, INL, and ONL of AD patients (Figures 5B,C; Koronyo et al., 2017). More recently, Asanad and colleagues analyzed retinal atrophy morphometrically in the superior quadrants of postmortem retinas from 8 AD and 11 age-matched controls (Asanad et al., 2019b). Measurements were acquired along a distance of 4mm from the optic nerve on the supero-temporal (reaching the macular region) and supero-nasal sides. Significant retinal thinning was revealed in the NFL (∼40%), GCL (35%), IPL (∼20%), and both nuclear layers (25%) in AD patients. In the supero-temporal region, NFL thinning was more pronounced closer to the optic nerve, whereas the other retinal layers showed prominent thinning closer to the macula. However, all analyzed retinal layers showed consistent thinning throughout the supero-nasal retinal quadrant (Asanad et al., 2019b). Beyond these changes, several studies have demonstrated accumulation of Aβ in the lens of AD patients (Goldstein et al., 2003; Tian et al., 2014) as well as reductions in the choroid coat – the vascular layer of the eye – and offered insights into the retinal choroid as an oculovascular biomarker for Alzheimer’s disease (Tsai et al., 2014; Asanad et al., 2019a)."}

{"project":"0_colil","denotations":[{"id":"33041751-28814675-816586","span":{"begin":362,"end":366},"obj":"28814675"},{"id":"33041751-12699953-816589","span":{"begin":1263,"end":1267},"obj":"12699953"},{"id":"33041751-24688166-816590","span":{"begin":1282,"end":1286},"obj":"24688166"},{"id":"33041751-24398104-816591","span":{"begin":1478,"end":1482},"obj":"24398104"}],"text":"These findings were corroborated in another study, which indicated a substantial loss of retinal cells at sites of Aβ deposition (Figures 5A–D). When compared with age-matched cognitively normal controls, 22-29% retinal neuronal degeneration was detected by Nissl staining (n = 17 subjects) in the GCL, INL, and ONL of AD patients (Figures 5B,C; Koronyo et al., 2017). More recently, Asanad and colleagues analyzed retinal atrophy morphometrically in the superior quadrants of postmortem retinas from 8 AD and 11 age-matched controls (Asanad et al., 2019b). Measurements were acquired along a distance of 4mm from the optic nerve on the supero-temporal (reaching the macular region) and supero-nasal sides. Significant retinal thinning was revealed in the NFL (∼40%), GCL (35%), IPL (∼20%), and both nuclear layers (25%) in AD patients. In the supero-temporal region, NFL thinning was more pronounced closer to the optic nerve, whereas the other retinal layers showed prominent thinning closer to the macula. However, all analyzed retinal layers showed consistent thinning throughout the supero-nasal retinal quadrant (Asanad et al., 2019b). Beyond these changes, several studies have demonstrated accumulation of Aβ in the lens of AD patients (Goldstein et al., 2003; Tian et al., 2014) as well as reductions in the choroid coat – the vascular layer of the eye – and offered insights into the retinal choroid as an oculovascular biomarker for Alzheimer’s disease (Tsai et al., 2014; Asanad et al., 2019a)."}