PMC:7523471 / 69818-71119 JSONTXT

{"project":"TEST0","denotations":[{"id":"33041751-168-176-816717","span":{"begin":168,"end":172},"obj":"[\"21635964\"]"},{"id":"33041751-191-199-816718","span":{"begin":191,"end":195},"obj":"[\"26137497\"]"},{"id":"33041751-212-220-816719","span":{"begin":212,"end":216},"obj":"[\"29565290\"]"},{"id":"33041751-232-240-816720","span":{"begin":244,"end":248},"obj":"[\"26035762\"]"},{"id":"33041751-235-243-816721","span":{"begin":268,"end":272},"obj":"[\"26852158\"]"},{"id":"33041751-232-240-816722","span":{"begin":303,"end":307},"obj":"[\"23768921\"]"},{"id":"33041751-98-106-816723","span":{"begin":867,"end":871},"obj":"[\"32043162\"]"}],"text":"In general, retinal inflammation is implicated in multiple traditional retinal vascular and neurodegenerative disorders, including diabetic retinopathy (Tang and Kern, 2011; Semeraro et al., 2015; Rubsam et al., 2018), AMD (Knickelbein et al., 2015; Kauppinen et al., 2016), and glaucoma (Vohra et al., 2013). During the onset of disease pathogenesis, retinal inflammation is usually triggered by an imbalance of pro- versus anti-inflammatory molecules. This can be evoked by a wide spectrum of pathogenic pathways, including overproduction of reactive oxygen species, activation of NF-κB or protein kinase C pathways, inflammasome or microglial activation, advanced glycation end products, or shear pressure and leukocyte invasion due to retinal microvascular damage. In this context, the recent discovery of early retinal pericyte loss in MCI patients (Shi et al., 2020) suggests an early BRB disturbance and perhaps retinal microvascular leakage in AD pathogenesis that may be implicated in retinal inflammation. Future studies should evaluate BRB leakage and the potential relationship with imbalanced retinal inflammatory pathway activation and brain inflammation in AD. Findings from such studies could lead to the discovery of novel retinal biomarkers to facilitate AD detection and monitoring."}

{"project":"2_test","denotations":[{"id":"33041751-21635964-38666503","span":{"begin":168,"end":172},"obj":"21635964"},{"id":"33041751-26137497-38666504","span":{"begin":191,"end":195},"obj":"26137497"},{"id":"33041751-29565290-38666505","span":{"begin":212,"end":216},"obj":"29565290"},{"id":"33041751-26035762-38666506","span":{"begin":244,"end":248},"obj":"26035762"},{"id":"33041751-26852158-38666507","span":{"begin":268,"end":272},"obj":"26852158"},{"id":"33041751-23768921-38666508","span":{"begin":303,"end":307},"obj":"23768921"},{"id":"33041751-32043162-38666509","span":{"begin":867,"end":871},"obj":"32043162"}],"text":"In general, retinal inflammation is implicated in multiple traditional retinal vascular and neurodegenerative disorders, including diabetic retinopathy (Tang and Kern, 2011; Semeraro et al., 2015; Rubsam et al., 2018), AMD (Knickelbein et al., 2015; Kauppinen et al., 2016), and glaucoma (Vohra et al., 2013). During the onset of disease pathogenesis, retinal inflammation is usually triggered by an imbalance of pro- versus anti-inflammatory molecules. This can be evoked by a wide spectrum of pathogenic pathways, including overproduction of reactive oxygen species, activation of NF-κB or protein kinase C pathways, inflammasome or microglial activation, advanced glycation end products, or shear pressure and leukocyte invasion due to retinal microvascular damage. In this context, the recent discovery of early retinal pericyte loss in MCI patients (Shi et al., 2020) suggests an early BRB disturbance and perhaps retinal microvascular leakage in AD pathogenesis that may be implicated in retinal inflammation. Future studies should evaluate BRB leakage and the potential relationship with imbalanced retinal inflammatory pathway activation and brain inflammation in AD. Findings from such studies could lead to the discovery of novel retinal biomarkers to facilitate AD detection and monitoring."}

{"project":"0_colil","denotations":[{"id":"33041751-21635964-816717","span":{"begin":168,"end":172},"obj":"21635964"},{"id":"33041751-26137497-816718","span":{"begin":191,"end":195},"obj":"26137497"},{"id":"33041751-29565290-816719","span":{"begin":212,"end":216},"obj":"29565290"},{"id":"33041751-26035762-816720","span":{"begin":244,"end":248},"obj":"26035762"},{"id":"33041751-26852158-816721","span":{"begin":268,"end":272},"obj":"26852158"},{"id":"33041751-23768921-816722","span":{"begin":303,"end":307},"obj":"23768921"},{"id":"33041751-32043162-816723","span":{"begin":867,"end":871},"obj":"32043162"}],"text":"In general, retinal inflammation is implicated in multiple traditional retinal vascular and neurodegenerative disorders, including diabetic retinopathy (Tang and Kern, 2011; Semeraro et al., 2015; Rubsam et al., 2018), AMD (Knickelbein et al., 2015; Kauppinen et al., 2016), and glaucoma (Vohra et al., 2013). During the onset of disease pathogenesis, retinal inflammation is usually triggered by an imbalance of pro- versus anti-inflammatory molecules. This can be evoked by a wide spectrum of pathogenic pathways, including overproduction of reactive oxygen species, activation of NF-κB or protein kinase C pathways, inflammasome or microglial activation, advanced glycation end products, or shear pressure and leukocyte invasion due to retinal microvascular damage. In this context, the recent discovery of early retinal pericyte loss in MCI patients (Shi et al., 2020) suggests an early BRB disturbance and perhaps retinal microvascular leakage in AD pathogenesis that may be implicated in retinal inflammation. Future studies should evaluate BRB leakage and the potential relationship with imbalanced retinal inflammatory pathway activation and brain inflammation in AD. Findings from such studies could lead to the discovery of novel retinal biomarkers to facilitate AD detection and monitoring."}