Systemic epigallocatechin gallate protects against retinal degeneration and hepatic oxidative stress in the P23H-1 rat

Retinitis pigmentosa(RP) is a group of inherited retinal disorders that lead to photoreceptor loss.RP has been reported to be related to oxidative stress,autophagy,and inflammation.(-)-Epigallocatechin gallate(EGCG),the most abundant catechin-based flavonoid in green tea leaves,has significant antioxidant,anti-carcinogenic,antimicrobial,and neuroprotective properties.EGCG,given its low molecular weight and hydrophilic properties,can cross the blood-retinal barrier and is able to reach different ocular tissues such as the lens,cornea,and retina.EGCG has been shown to provide retinal protection against ischemia;sodium nitroprusside-,N-methyl-D-aspartate-,lipopolysaccharide-,light-,sodium iodate-,or H2 O2-induced damage and diabetic retinopathy.This suggests that systemic EGCG administration has the potential to protect against retinal degenerative or neurodegenerative diseases such as RP.The aim of this work was to investigate whether EGCG can protect against RP progression in the animal P23 H line 1,the model of RP.Albino P23 H rats were crossed with pigmented Long Evans rats to produce offspring exhibiting the clinical features of RP.Pigmented P23 H rats were treated via intraperitoneal injection with saline or EGCG at a dose of 25 mg/kg every week from P100 to P160 and then compared to wild-type Long Evans rats.Rats treated with EGCG showed better visual and retinal electrical function with increased contrast sensitivity and b-wave values compared with those observed in P23 H rats treated with vehicle.EGCG reduced lipid peroxidation and increased total antioxidant capacity and catalase and superoxide dismutase activities.No differences were observed in visual acuity,nitrate levels,nitrite levels or glutathione S-transferase activity.In conclusion,EGCG not only reduced the loss of visual function in P23 H rats but also improved the levels of antioxidant enzymes and reduced oxidative damage.This study was approved by the Institutional Animal Care and Use Committee(CEICA) from the University of Zaragoza under project license PI12/14 on July 11,2014.

Current and future therapeutic strategies for the treatment of retinal neurodegenerative diseases

The complex and mostly multiple and unknown aetiology of neurodegenerative diseases always give way to an intricate scenario of dying tissue that involves multiple cell mediators and cell types.All neurodegenerative diseases of the central nervous system(CNS)share common mechanisms,regardless their origin:oxidative stress,neuroinflammation and cell death.Accordingly,retinal degenerative diseases,with or without a genetic cause,as retinitis pigmentosa(RP),glaucoma,agerelated macular degeneration(AMD)or diabetic retinopathy(DR)do not differ in their basic mechanisms of cell death neither one to another,nor from those observed in other CNS diseases as Parkinson’s or Alzheimer’s(Cuenca et al.,2014).Indeed,the therapeutic findings should be able to be more or less easily extrapolated between these conditions,as far as they are directed to common dartboards.

Starburst amacrine cells,involved in visual motion perception,lose their synaptic input from dopaminergic amacrine cells and degenerate in Parkinson’s disease patients

Background The main clinical symptoms characteristic of Parkinson’s disease(PD)are bradykinesia,tremor,and other motor deficits.However,non-motor symptoms,such as visual disturbances,can be identified at early stages of the disease.One of these symptoms is the impairment of visual motion perception.Hence,we sought to determine if the starburst amacrine cells,which are the main cellular type involved in motion direction selectivity,are degenerated in PD and if the dopaminergic system is related to this degeneration.Methods Human eyes from control(n=10)and PD(n=9)donors were available for this study.Using immunohistochemistry and confocal microscopy,we quantified starburst amacrine cell density(choline acetyltransferase[ChAT]-positive cells)and the relationship between these cells and dopaminergic amacrine cells(tyrosine hydroxylase-positive cells and vesicular monoamine transporter-2-positive presynapses)in cross-sections and wholemount retinas.Results First,we found two different ChAT amacrine populations in the human retina that presented different ChAT immunoreactivity intensity and different expression of calcium-binding proteins.Both populations are affected in PD and their density is reduced compared to controls.Also,we report,for the first time,synaptic contacts between dopaminergic amacrine cells and ChAT-positive cells in the human retina.We found that,in PD retinas,there is a reduction of the dopaminergic synaptic contacts into ChAT cells.Conclusions Taken together,this work indicates degeneration of starburst amacrine cells in PD related to dopaminergic degeneration and that dopaminergic amacrine cells could modulate the function of starburst amacrine cells.Since motion perception circuitries are affected in PD,their assessment using visual tests could provide new insights into the diagnosis of PD.

Correction:Starburst amacrine cells,involved in visual motion perception,lose their synaptic input from dopaminergic amacrine cells and degenerate in Parkinson’s disease patients

Correction:Translational Neurodegeneration(2023)12:17(2023)https://doi.org/10.1186/s40035-023-00348-y Following publication of the original article[1],the authors reported an error in the article title.Following publication of the original article[1],the authors reported an error in the article title.“Lose”was mistakenly typed as“loose”in the original title.The correct title should read:Starburst amacrine cells,involved in visual motion perception,lose their synaptic input from dopaminergic amacrine cells and degenerate in Parkinson’s disease patients.