AIM:To investigate the effect of 0.01%low-concentration atropine(LA)on quantitative contrast sensitivity function(qCSF)in children with myopia.METHODS:This paired case-control study included 90 eyes of 58 children who...AIM:To investigate the effect of 0.01%low-concentration atropine(LA)on quantitative contrast sensitivity function(qCSF)in children with myopia.METHODS:This paired case-control study included 90 eyes of 58 children who were sex-,age-,and refractionmatched and equally divided into two groups:the 0.01%LA group had undergone 6mo use of daily 0.01%atropine and control group was naïve to LA.Routine ophthalmic examinations and qCSF test without refractive correction were performed.Two groups were compared in monocular and binocular qCSF parameters,including the area under logCSF,CSF acuity,and contrast sensitivity(CS)at 1.0-18.0 cycle per degree(cpd).RESULTS:In the monocular comparison,the CSF acuity of the LA group was significantly higher than that of the control group(7.58±5.51 vs 6.37±4.22 cpd,P<0.05).The subgroup analysis showed that in the 6-9y group,CSF acuity was significantly higher in the LA group than the control group(8.76±6.19 vs 6.54±4.25 cpd,P<0.05),and in the Female group,low refraction sphere group,and high refraction cylinder group,the CS at high spatial frequencies(12.0 and 18.0 cpd)were significantly higher in the LA group than in the control group(all P<0.05).In the binocular test,CSF acuity and CS at 12.0 cpd were significantly higher in the LA group than in the control group(10.95±7.00 vs 8.65±5.12 cpd;0.17±0.33 vs 0.06±0.16,respectively;both P<0.05).CONCLUSION:Use of LA may result in improved CS in children with early onset myopia.展开更多
Brain-derived neurotrophic factor(BDNF)plays an important role in neurodevelopment,synaptic plasticity,learning and memory,and in preventing neurodegeneration.Despite decades of investigations into downstream signalin...Brain-derived neurotrophic factor(BDNF)plays an important role in neurodevelopment,synaptic plasticity,learning and memory,and in preventing neurodegeneration.Despite decades of investigations into downstream signaling cascades and changes in cellular processes,the mechanisms of how BDNF reshapes circuits in vivo remain unclear.This informational gap partly arises from the fact that the bulk of studies into the molecular actions of BDNF have been performed in dissociated neuronal cultures,while the majority of studies on synaptic plasticity,learning and memory were performed in acute brain slices or in vivo.A recent study by Bowling-Bhattacharya et al.,measured the proteomic changes in acute adult hippocampal slices following treatment and reported changes in proteins of neuronal and non-neuronal origin that may in concert modulate synaptic release and secretion in the slice.In this paper,we place these findings into the context of existing literature and discuss how they impact our understanding of how BDNF can reshape the brain.展开更多
Glaucoma, the world's leading cause of irreversible blindness, is a condition for which elevated intraocular pressure is currently the only modifiable risk factor. However, the disorder can continue to progress ev...Glaucoma, the world's leading cause of irreversible blindness, is a condition for which elevated intraocular pressure is currently the only modifiable risk factor. However, the disorder can continue to progress even at reduced intraocular pressure. This indicates additional key factors that contribute to the etiopathogenesis. There has been a growing amount of literature suggesting glaucoma as a neurodegenerative disease of the visual system. However, it remains debatable whether the observed pathophysiological conditions are causes or consequences. This review summarizes recent in vivo imaging studies that helped advance the understanding of early glaucoma involvements and disease progression in the brains of humans and experimental animal models. In particular, we focused on the non-invasive detection of early structural and functional brain changes before substantial clinical visual field loss in glaucoma patients; the eye-brain interactions across disease severity; the metabolic changes occurring in the brain's visual system in glaucoma; and, the widespread brain involvements beyond the visual pathway as well as the potential behavioral relevance. If the mechanisms of glaucomatous brain changes are reliably identified, novel neurotherapeutics that target parameters beyond intraocular pressure lowering can be the promise of the near future, which would lead to reduced prevalence of this irreversible but preventable disease.展开更多
Optic nerve health is essential for proper function of the visual system.However,the pathophysiology of certain neurodegenerative disease processes affecting the optic nerve,such as glaucoma,is not fully understood.Re...Optic nerve health is essential for proper function of the visual system.However,the pathophysiology of certain neurodegenerative disease processes affecting the optic nerve,such as glaucoma,is not fully understood.Recently,it was hypothesized that a lack of proper clearance of neurotoxins contributes to neurodegenerative diseases.The ability to clear metabolic waste is essential for tissue homeostasis in mammals,including humans.While the brain lacks the traditional lymphatic drainage system identified in other anatomical regions,there is growing evidence of a glymphatic system in the central nervous system,which structurally includes the optic nerve.Named to acknowledge the supportive role of astroglial cells,this perivascular fluid drainage system is essential to remove toxic metabolites from the central nervous system.Herein,we review existing literature describing the physiology and dysfunction of the glymphatic system specifically as it relates to the optic nerve.We summarize key imaging studies demonstrating the existence of a glymphatic system in the optic nerves of wild-type rodents,aquaporin 4-null rodents,and humans;glymphatic imaging studies in diseases where the optic nerve is impaired;and current evidence regarding pharmacological and lifestyle interventions that may help promote glymphatic function to improve optic nerve health.We conclude by highlighting future research directions that could be applied to improve imaging detection and guide therapeutic interventions for diseases affecting the optic nerve.展开更多
基金Supported by National Key Research and Development Program of China(No.2023YFA0915000)。
文摘AIM:To investigate the effect of 0.01%low-concentration atropine(LA)on quantitative contrast sensitivity function(qCSF)in children with myopia.METHODS:This paired case-control study included 90 eyes of 58 children who were sex-,age-,and refractionmatched and equally divided into two groups:the 0.01%LA group had undergone 6mo use of daily 0.01%atropine and control group was naïve to LA.Routine ophthalmic examinations and qCSF test without refractive correction were performed.Two groups were compared in monocular and binocular qCSF parameters,including the area under logCSF,CSF acuity,and contrast sensitivity(CS)at 1.0-18.0 cycle per degree(cpd).RESULTS:In the monocular comparison,the CSF acuity of the LA group was significantly higher than that of the control group(7.58±5.51 vs 6.37±4.22 cpd,P<0.05).The subgroup analysis showed that in the 6-9y group,CSF acuity was significantly higher in the LA group than the control group(8.76±6.19 vs 6.54±4.25 cpd,P<0.05),and in the Female group,low refraction sphere group,and high refraction cylinder group,the CS at high spatial frequencies(12.0 and 18.0 cpd)were significantly higher in the LA group than in the control group(all P<0.05).In the binocular test,CSF acuity and CS at 12.0 cpd were significantly higher in the LA group than in the control group(10.95±7.00 vs 8.65±5.12 cpd;0.17±0.33 vs 0.06±0.16,respectively;both P<0.05).CONCLUSION:Use of LA may result in improved CS in children with early onset myopia.
基金supported by NIH grants NS034007 and NS047384supported by NIH grants NS21072,and HD23315supported by funds from the Department of Biotechnology,Government of India and the Shanta Wadhwani Foundation
文摘Brain-derived neurotrophic factor(BDNF)plays an important role in neurodevelopment,synaptic plasticity,learning and memory,and in preventing neurodegeneration.Despite decades of investigations into downstream signaling cascades and changes in cellular processes,the mechanisms of how BDNF reshapes circuits in vivo remain unclear.This informational gap partly arises from the fact that the bulk of studies into the molecular actions of BDNF have been performed in dissociated neuronal cultures,while the majority of studies on synaptic plasticity,learning and memory were performed in acute brain slices or in vivo.A recent study by Bowling-Bhattacharya et al.,measured the proteomic changes in acute adult hippocampal slices following treatment and reported changes in proteins of neuronal and non-neuronal origin that may in concert modulate synaptic release and secretion in the slice.In this paper,we place these findings into the context of existing literature and discuss how they impact our understanding of how BDNF can reshape the brain.
基金supported by the National Institutes of Health R01-EY028125(Bethesda,MD,USA)(to KCC)BrightFocus Foundation G2013077 and G2016030(Clarksburg,MD,USA)(to KCC)Research to Prevent Blindness/Stavros Niarchos Foundation International Research Collaborators Award(New York,NY,USA)(to KCC)
文摘Glaucoma, the world's leading cause of irreversible blindness, is a condition for which elevated intraocular pressure is currently the only modifiable risk factor. However, the disorder can continue to progress even at reduced intraocular pressure. This indicates additional key factors that contribute to the etiopathogenesis. There has been a growing amount of literature suggesting glaucoma as a neurodegenerative disease of the visual system. However, it remains debatable whether the observed pathophysiological conditions are causes or consequences. This review summarizes recent in vivo imaging studies that helped advance the understanding of early glaucoma involvements and disease progression in the brains of humans and experimental animal models. In particular, we focused on the non-invasive detection of early structural and functional brain changes before substantial clinical visual field loss in glaucoma patients; the eye-brain interactions across disease severity; the metabolic changes occurring in the brain's visual system in glaucoma; and, the widespread brain involvements beyond the visual pathway as well as the potential behavioral relevance. If the mechanisms of glaucomatous brain changes are reliably identified, novel neurotherapeutics that target parameters beyond intraocular pressure lowering can be the promise of the near future, which would lead to reduced prevalence of this irreversible but preventable disease.
基金supported by National Institutes of Health,No.R01-EY028125Bright Focus Foundation,No.G2019103+2 种基金Feldstein Medical FoundationResearch to Prevent Blindness/Stavros Niarchos Foundation International Research Collaborators Awardan unrestricted grant from Research to Prevent Blindness to NYU Langone Health Department of Ophthalmology(to KCC)。
文摘Optic nerve health is essential for proper function of the visual system.However,the pathophysiology of certain neurodegenerative disease processes affecting the optic nerve,such as glaucoma,is not fully understood.Recently,it was hypothesized that a lack of proper clearance of neurotoxins contributes to neurodegenerative diseases.The ability to clear metabolic waste is essential for tissue homeostasis in mammals,including humans.While the brain lacks the traditional lymphatic drainage system identified in other anatomical regions,there is growing evidence of a glymphatic system in the central nervous system,which structurally includes the optic nerve.Named to acknowledge the supportive role of astroglial cells,this perivascular fluid drainage system is essential to remove toxic metabolites from the central nervous system.Herein,we review existing literature describing the physiology and dysfunction of the glymphatic system specifically as it relates to the optic nerve.We summarize key imaging studies demonstrating the existence of a glymphatic system in the optic nerves of wild-type rodents,aquaporin 4-null rodents,and humans;glymphatic imaging studies in diseases where the optic nerve is impaired;and current evidence regarding pharmacological and lifestyle interventions that may help promote glymphatic function to improve optic nerve health.We conclude by highlighting future research directions that could be applied to improve imaging detection and guide therapeutic interventions for diseases affecting the optic nerve.
