Details about canine genetic testing for the product: Progressive Retinal Atrophy, Progressive Rod-Cone Degeneration, for the breed: Lakeland Terrier.

Mice with hereditary retinal degeneration have provided excellent models for human disease of the biochemical and physiological events occurring in retinal degeneration. Since a number of mouse models are available for other human conditions, more mouse retinal degenerations would be expected to be known; however, finding new models has proved difficult since the search has usually involved laborious histologic screening. We applied the clinical technique of indirect ophthalmoscopy to screen mice for retinal degeneration and then used electroretinography and histology to determine whether true retinal degeneration was present. A Dawson-Trick-Litzkow microfiber corneal electrode was used to record the electroretinogram since the fiber does not occlude the pupil in these small eyes. Normal control values were developed. As an example of the success of the technique, one strain, lethal spot (ls) on indirect ophthalmoscopy appeared to have a retinal degeneration, but these mice had a normal

Histologic analysis of retinal tissue has been considered the gold standard for characterizing retinal degeneration and assessing the efficacy of potential treatments for AMD and inherited retinal dystrophies in the RCS rat.8,12,26,43-46 However, histologic processing precludes the ability to perform longitudinal analysis, thus increasing the number of animals required for long-term studies. In addition, artifacts from postmortem processing are unavoidable, including fixation and dehydration, which can alter layer thicknesses and mask features of in vivo disease progression. Noninvasive, high-resolution SD-OCT imaging offers an alternative in vivo approach to obtaining structural measurements of disease progression.30 Spectral-domain OCT imaging has been validated in multiple mouse (Rho−/−, Rpe65−/−, rd1, rd10) and rat (Rho P23H) inherited retinal degeneration models.32-34 These studies have consistently reported that SD-OCT is able to capture morphologic changes during disease ...

We report isolating the Drosophila retinal degeneration E (rdgE) mutation. The hypomorphic rdgE1 allele causes rapid photoreceptor degeneration in light and a slower rate of degeneration when the flies are raised in constant darkness. The rdgE1 flies exhibited an electrophysiological light response that decreased with age, coinciding with the degeneration. This suggests that degeneration caused the loss of the light response. We determined that the ninaE (rhodopsin) mutation, but not norpA [phospholipase C (PLC)], slowed the rdgE-dependent degeneration. This was consistent with the light-enhanced degeneration, but revealed that the degeneration is independent of the PLC-mediated phototransduction cascade. Transmission electron microscopy revealed that rdgE1 photoreceptors exhibited a number of vesicular transport defects including unpacking/vesiculation of rhabdomeres, endocytosis of novel vesicles by photoreceptors, a buildup of very large multivesicular bodies, and an increased amount of rough ...

T17M rhodopsin expression in rod photoreceptors leads to severe retinal degeneration and is associated with the activation of ER stress related Unfolded Protein Response (UPR) signaling. Here, we show a novel role of a UPR transcription factor, ATF4, in photoreceptor cellular pathology. We demonstrated a pro-death role for ATF4 overexpression during autosomal dominant retinitis pigmentosa (ADRP). Based on our results in ATF4 knockout mice and adeno-associated viral (AAV) delivery of ATF4 to the retina, we validated a novel therapeutic approach targeting ATF4 over the course of retinal degeneration. In T17M rhodopsin retinas, we observed ATF4 overexpression concomitantly with reduction of p62 and elevation of p53 levels. These molecular alterations, together with increased CHOP and caspase-3/7 activity, possibly contributed to the mechanism of photoreceptor cell loss. Conversely, ATF4 knockdown retarded retinal degeneration in 1-month-old T17M Rhodopsin mice and promoted photoreceptor survival, as

PURPOSE: To evaluate the retinal degeneration of the motor neuron degeneration (mnd) mouse, and to confirm its inheritance pattern and gene location. METHODS: In screening the mnd/mnd mouse for ocular disease, a retinal degeneration was found that was evaluated by serial electroretinography, histology, electron microscopy, indirect ophthalmoscopy, and genetic and linkage analysis. RESULTS: In homozygous mnd mice, photoreceptor and outer nuclear layers show cell loss by 5 weeks after birth. By 2 months, the peripheral retina is preferentially thinner than central retina, and by 6 months the entire retina is reduced in thickness. The electroretinogram was extinguished by 6 months. Transmission electron microscopy at 3 and 6 months showed distinct cytoplasmic inclusions characteristic of the curvilinear profiles seen in human ceroid lipofuscinosis. Genetic analyses show that the retinal degeneration in mnd mice is inherited as a single autosomal gene with recessive expression, and a three

4 Stages Of Lumbar Degeneration - Model - Get the lowest price on 4 Stages Of Lumbar Degeneration - Model, online at AllegroMedical.com.

In this study, we have investigated the retinal degeneration in a mouse line identified in a recessive ENU screen. This is the first mouse model of IDH3A-related chronic retinal degeneration described, and closely mirrors the phenotype observed in patients. However, is not possible to model the pseudocoloboma of the macula seen in human patients in mice, as they lack a macula. Through the course of the investigation, we confirmed the genetic source of the phenotype to be a missense mutation in the Idh3a gene. The amino acid mutated in the Idh3aE229K mouse is within the highly conserved nucleotide-binding domain observed in both NAD- and NADP-dependent dehydrogenases of animals, including Caenorhabditis elegans and Drosophila (Pierrache et al., 2017). E229 is close to the amino acid critical for binding the divalent cation necessary for activity (D233), and is within a short segment of β-sheet (Ma et al., 2017b).. Mutation of such a highly conserved amino acid residue in an important part of the ...

PRA-prcd is an inherited degenerative disease that affects a dogs vision and can lead to complete blindness. Get an accurate diagnosis through EasyDNAs Dog PRA-prcd Test, starting at only €79

A pain medicine that potently activates a receptor vital to a healthy retina assist preserve vision in a model of severe retinal degeneration.

The eye uses vitamin A as a cofactor to sense light, during this process a fraction of vitamin A dimerizes forming vitamin A dimers. A striking chemical signature of retinas undergoing degeneration in major eye diseases such as age-related macular degeneration (AMD) and Stargardt disease, is the accumulation of these dimers in the retinal pigment epithelium (RPE) and Bruchs membrane (BM). However, it is not known whether dimers of vitamin A are merely secondary symptoms or primary insults that drive degeneration. Here, we present a chromatography free method to prepare gram quantities of the vitamin A dimer, A2E, and show that intravenous administration of A2E to the rabbit results in retinal degeneration. A2E damaged photoreceptors and RPE cells, triggered inflammation, induced remolding of the choroidal vasculature, and triggered a decline in the retinas response to light. Data suggest that vitamin A dimers are not bystanders, but can be primary drivers of retinal degeneration. Thus, ...

Gene correction is a valuable strategy for treating inherited retinal degenerative diseases, a major cause of irreversible blindness worldwide. Single gene defects cause the majority of these retinal dystrophies. Gene augmentation holds great promise if delivered early in the course of the disease, however, many patients carry mutations in genes too large to be packaged into adeno-associated viral vectors and some, when overexpressed via heterologous promoters, induce retinal toxicity. In addition to the aforementioned challenges, some patients have sustained significant photoreceptor cell loss at the time of diagnosis, rendering gene replacement therapy insufficient to treat the disease. These patients will require cell replacement to restore useful vision. Fortunately, the advent of induced pluripotent stem cell and CRISPR-Cas9 gene editing technologies affords researchers and clinicians a powerful means by which to develop strategies to treat patients with inherited retinal dystrophies. In ...

We used quantitative real-time PCR to examine the expression of 112 genes related to retinal function and/or belonging to known pro-apoptotic, cell survival, and autophagy pathways during photoreceptor degeneration in three early-onset canine models of human photoreceptor degeneration, rod cone dysplasia 1 (rcd1), X-linked progressive retinal atrophy 2 (xlpra2), and early retinal degeneration (erd), caused respectively, by mutations in PDE6B, RPGRORF15, and STK38L. Notably, we found that expression and timing of differentially expressed (DE) genes correlated with the cell death kinetics. Gene expression profiles of rcd1 and xlpra2 were similar; however rcd1 was more severe as demonstrated by the results of the TUNEL and ONL thickness analyses, a greater number of genes that were DE, and the identification of altered expression that occurred at earlier time points. Both diseases differed from erd, where a smaller number of genes were DE. Our studies did not highlight the potential involvement of

During a 2-year period, 31 cases of a hereditary retinal degeneration in dogs bred in India were found mainly suspected for progressive retinal atrophy (PRA) with typical history of initial nyctalopia followed by hemeralopia. Out of 31 PRA suspected dogs, 8 dogs (26%) were from the age group of 1-5 years, 15 (48%) 6-10 years and the rest (26%) 11-15 years. The most predominant breed was Spitz (18 dogs, 58%). Detailed ophthalmologic examinations included Schirmers tear test, fluorescein stain, applanation tonometry, slit lamp biomicroscopy and ocular ultrasound in appropriate cases. Ophthalmoscopic and fundoscopic changes included hyperreflectivity and discoloration of the tapetal area, marked attenuation of retinal vessels, depigmentation in non-tapetal area and optic disc atrophy with scalloped borders. Electroretinograms (ERG) recorded in 13 PRA-affected cases revealed non-recordable extinguished (flatline) ERG responses. A reduction mainly of a- and b-wave amplitudes in the ERG indicated a

We first evaluated the phosphorylation state of Akt at Ser-473, the site of phosphorylation by MAPKAPK-2, which has been shown to be critical for the generation of high levels of Akt enzyme activity. 15 32 33 Several other kinases have also been reported to phosphorylate Akt at Ser-473, including integrin-linked kinase (ILK), 34 35 36 3-phosphoinositide-dependent kinase-1 (PDK-1) 35 and DNA-dependent protein kinase (DNA-PK). 37 Our data showed two distinct phases of Ser-473 Akt modulation during photoreceptor degeneration: the first one was characterized by the inactivation of Akt, and extended from early onset (13 days) to the peak of photoreceptor apoptosis (15 days), and the following one displayed a striking Akt activation during the period when most photoreceptors have degenerated. The fact that Akt activation levels were decreased and no immunoreactivity of the active form was detected at the photoreceptor level, strongly suggests that the Akt survival signaling pathway was inhibited ...

We have demonstrated that adult bone marrow-derived Lin- HSCs exert profound vasculotrophic and neurotrophic effects when injected intravitreally into mice with retinal degenerative disease. This rescue effect persists for up to 6 months after treatment and is most efficacious when the Lin- HSCs are injected prior to complete retinal degeneration (up to 16 days after birth in mice that ordinarily exhibit practically complete ONL degeneration by 30 days postnatally). This rescue is observed in two mouse models of retinal degeneration and, remarkably, can be accomplished with adult hBM-derived HSCs when the recipient is an immunodeficient rodent with retinal degeneration (e.g., the SCID mouse) or when the donor is itself a mouse with retinal degeneration. PRs in the normal mouse retina are predominantly rods, but the ONL observed after rescue with Lin- HSCs contains predominantly cones. While several recent reports have described a partial phenotypic rescue in mice or dogs with retinal ...

While the diagnosis of retinal degeneration is made by ophthalmoscopy and/or electroretinography, genetic testing for PRA can be useful for breeders to identify not only affected animals, but those that are genetic carriers for the disease. This type of diagnosis is essential to eliminate carriers from the breeding population. For more information on genetic testing, visit Optigen.com.. Unfortunately, there is no proven treatment for any form of retinal degeneration. These conditions are painless and, in most cases, loss of vision progresses slowly and pets adjust to this handicap remarkably well. Animals which are irreversibly blind can live a normal lifespan and have an excellent quality of life provided some extra care by their owners. It is important to recognize that loss of vision does not represent the same handicap for our pets as it would for us. For us, blindness would mean an inability to read or drive a car and a loss of independence. Our pets are already (happily) dependent on us. ...

Although many different mutations in humans and Drosophila cause retinal degeneration, in most cases, a molecular mechanism for the degeneration has not been found. We now demonstrate the existence of stable, persistent complexes between rhodopsin and its regulatory protein arrestin in several diffe …

Post-transcriptional gene silencing (PTGS) agents such as ribozymes, RNAi and antisense have substantial potential for gene therapy of human retinal degenerations. These technologies are used to knockdown a specific target RNA and its cognate protein. The disease target mRNA may be a mutant mRNA causing an autosomal dominant retinal degeneration or a normal mRNA that is overexpressed in certain diseases. All PTGS technologies depend upon the initial critical annealing event of the PTGS ligand to the target RNA. This event requires that the PTGS agent is in a conformational state able to support hybridization and that the target have a large and accessible single-stranded platform to allow rapid annealing, although such platforms are rare. We address the biocomplexity that currently limits PTGS therapeutic development with particular emphasis on biophysical variables that influence cellular performance. We address the different strategies that can be used for development of PTGS agents intended for

Retinal Degeneration Global Clinical Trials Review, H2, 2016 provides an overview of Retinal Degeneration clinical trials scenario. This report provides to

Retinal Degeneration - This page provide you with a great set of 33 carefully selected sites about: retinal degeneration. All links have been manually verified!

Photoreceptor cells found in the back of our eyes convert light into signals that allow us to see. Death of these cells and the cells that nourish them, called RPE cells, is termed retinal degeneration and is characteristic of blinding diseases such as age-related macular degeneration (AMD) and retinitis pigmentosa. Millions of people worldwide suffer varying degrees of vision-loss due to these irreversible eye conditions, in fact, the number of individuals suffering from AMD is expected to reach ~288 million globally by 2040. The process of cell-death is a programmed event that directs proteins in our cells to take on ?executioner? roles. Over the past decade great leaps have been made in identifying these executioner proteins and in understanding the pathways that lead to their activation. There are a wide range of causes behind cell-death in the eye, but ultimately the end-point for each is photoreceptor cell death. Identifying unifying pro-death or pro-survival traits in these diseases has ...

Inherited retinal degenerations afflict 1 in 3,500 individuals and are a heterogeneous group of diseases that result in profound vision loss, usually the result of retinal neuronal apoptosis. Atrophic changes in the retinal vasculature are also observed in many of these degenerations. While it is thought that this atrophy is secondary to diminished metabolic demand in the face of retinal degeneration, the precise relationship between the retinal neuronal and vascular degeneration is not clear. In this study we demonstrate that whenever a fraction of mouse or human adult bone marrow-derived stem cells (lineage-negative hematopoietic stem cells [Lin- HSCs]) containing endothelial precursors stabilizes and rescues retinal blood vessels that would ordinarily completely degenerate, a dramatic neurotrophic rescue effect is also observed. Retinal nuclear layers are preserved in 2 mouse models of retinal degeneration, rd1 and rd10, and detectable, albeit severely abnormal, electroretinogram recordings ...

To diagnose PRD, the veterinary ophthalmologist examines the retina with an instrument called an indirect ophthalmoscope. Changes in the retinal blood vessel pattern, the optic nerve head and the reflective substance within the dogs eye (called the tapetum) are classic signs of PRD.. However, PRD will progress at different rates in different breeds. In some breeds PRD causes little or no early changes, and the eyes of these dogs may appear normal until they are in the later stages of the disease. This variation makes it difficult for the vet to determine just how long any particular dog will continue seeing.. There is no possible treatment for PRD, although a number of vitamin therapies have been suggested. At this time, none of the vitamin treatments have been scientifically proven to be effective, so use of vitamins must be deemed a naturopathic remedy rather than a medical treatment.. Cataracts may occur in some patients with PRD, and generally occur later in the disease. Formation of ...

TY - JOUR. T1 - Neuroprotective role of retinal SIRT3 against acute photo-stress. AU - Ban, Norimitsu. AU - Ozawa, Yoko. AU - Osada, Hideto. AU - Lin, Jonathan B.. AU - Toda, Eriko. AU - Watanabe, Mitsuhiro. AU - Yuki, Kenya. AU - Kubota, Shunsuke. AU - Apte, Rajendra S.. AU - Tsubota, Kazuo. PY - 2017/12/1. Y1 - 2017/12/1. N2 - SIRT3 is a key regulator of mitochondrial reactive oxygen species as well as mitochondrial function. The retina is one of the highest energy-demanding tissues, in which the regulation of reactive oxygen species is critical to prevent retinal neurodegeneration. Although previous reports have demonstrated that SIRT3 is highly expressed in the retina and important in neuroprotection, function of SIRT3 in regulating reactive oxygen species in the retina is largely unknown. In this study, we investigated the role of retinal SIRT3 in a light-induced retinal degeneration model using SIRT3 knockout mice. We demonstrate that SIRT3 deficiency causes acute reactive oxygen species ...

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Sigma-Aldrich offers abstracts and full-text articles by [Satoshi Nojima, Toshihiko Toyofuku, Hiroyuki Kamao, Chie Ishigami, Jun Kaneko, Tatsusada Okuno, Hyota Takamatsu, Daisuke Ito, Sujin Kang, Tetsuya Kimura, Yuji Yoshida, Keiko Morimoto, Yohei Maeda, Atsushi Ogata, Masahito Ikawa, Eiichi Morii, Katsuyuki Aozasa, Junichi Takagi, Masayo Takahashi, Atsushi Kumanogoh].

Blindness is the inevitable end stage of retinal degeneration, meaning the irreversible loss of neurons in the retina. The two cell types in the retina that are generally associated with loss of vision in humans are either the ganglion cells or the photoreceptors. Loss of ganglion cells results in Glaucoma, a devastating disease affecting ~ 3 Millions in the United States alone. Loss PRs is associated with a large number of retinal degenerative diseases of which Age-related-Macular-Degeneration (AMD) is the most widespread with over 2 millions affected in the United States. Since photoreceptors account for ~75% of all cells in the retina, loss of photoreceptors results always in sever retinal degeneration. - Punzo Lab - UMASS Worcester - Retinal Degeneration - AMD rod - cone - rod-cone distropy

Contains the proceedings of the XVI International Symposium on Retinal Degeneration (RD2014), held July 13-18, 2014 at the Asilomar Conference Center in Pacific Grove, California. A majority of those

We have a new publication out (direct link, open access), Müller Cell Metabolic Chaos During Retinal Degeneration authored by Rebecca Pfeiffer, Robert Marc, Mineo Kondo, Hiroko Terasaki and myself.. Abstract:. Müller cells play a critical role in retinal metabolism and are among the first cells to demonstrate metabolic changes in retinal stress or disease. The timing, extent, regulation, and impacts of these changes are not yet known. We evaluated metabolic phenotypes of Müller cells in the degenerating retina.. Retinas harvested from wild-type (WT) and rhodopsin Tg P347L rabbits were fixed in mixed aldehydes and resin embedded for computational molecular phenotyping (CMP). CMP facilitates small molecule fingerprinting of every cell in the retina, allowing evaluation of metabolite levels in single cells.. CMP revealed signature variations in metabolite levels across Müller cells from TgP347L retina. In brief, neighboring Müller cells demonstrated variability in taurine, glutamate, ...

Retinal Degeneration symptoms include ... (239)390-3339 Florida Retina Center. Dr Patel is an Ophthalmologist in Bonita Springs Florida specializing in treating problems of the retina, macula and other eye problems

Diagnosis of retinal degeneration (costs for program #239645) ✔ University Hospital Hamburg-Eppendorf ✔ Department of Ophthalmology ✔ BookingHealth.com

Diagnostics of retinal degeneration (costs for program #112965) ✔ University Hospital of the Ludwig-Maximilians-University Munich ✔ Department of Ophthalmology ✔ BookingHealth.com

[email protected]. Research Focus: Although many patients worldwide suffer from retinal degenerations, there are currently no therapies for the successful treatment of most blinding diseases of the retina. Our work focuses on biochemical events and signaling cascades during retinal degenerations. The goal is to understand the molecular pathways induced by the disease-causing stimuli to develop strategies (neuroprotection, gene therapy) which may ultimately rescue vision in patients.. Current projects focus i) on intercellular signaling with special emphasis on the interaction between photoreceptors and Müller glia cells; ii) on leukemia inhibitory factor (LIF) with respect to its potential function as modulator of stem cell-like properties of Müller cells; iii) on the analysis of cone pathophysiology using a newly developed all-cone mouse; and iv) on acute and chronic hypoxia as potent modulators of photoreceptor survival and degeneration, respectively.. Keywords: Retinal degeneration, ...

Retinal degenerative diseases are one of many clinical causes of incurable and severe visional impairment. controlled, and lastly stored for clinicians and researchers attempting to gain access to individual tissue and check their own hypotheses. These precious individual posterior eye tissue could be useful for additional research reasons, epidemiological studies, and focus on validation of developed medications. Furthermore, this may be a guaranteeing and challenging substitute for get potential retinal stem and progenitor cells from various areas of the retina and may be a discovery in the foreseeable future delivery of ex girlfriend or boyfriend vivo prepared personalized (histocompatible) retinal tissues on scaffolds for transplantation reasons. Within this Perspective, we will consider the way the biorepositories could influence the near future approaches for retinal stem cell therapies. Significance Retinal degenerative illnesses are one of many causes of serious eyesight impairment and ...

Researchers based at the Jules Stein Eye Institute Retina Division and David Geffen School of Medicine, University of California, Los Angeles, have published the results of embryonic stem cell (hESC)-derived retinal pigment epithelium (RPE) cell treatments in two retinal degenerative diseases. The phase I/II open label studies were funded by Advanced Cell Technologies, Inc, a Massachusetts based clinical stage biotechnology company focused on regenerative medicine. Results, published online in the The Lancet, indicate that the primary end-points of safety and tolerability were met in addition to a potential positive impact on acuity noted by the investigators.. Back to previous ...

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Inherited retinal degenerative diseases (RDDs) are a heterogeneous group of disorders that constitute a major cause of vision loss in the world population. In m...

The Shiley Eye Institute is the only academic institution in the San Diego area with comprehensive programs for the clinical care of patients with eye disorders, cutting edge research on surgical techniques and treatments of eye diseases, education in the field of ophthalmology and innovative outreach to the community.

The easy accessibility of the eye and the established link between specific genetic defects and ocular disorders offer hope for using gene therapy to provide long-term therapeutic benefit. Two reports in the current issue of Human Gene Therapy, a peer-reviewed journal published by Mary Ann Liebert Inc., describe the effective replacement of a human gene to preserve photoreceptor function in a mouse model of severe retinal degeneration.

Progressive loss of vision. Description: Progressive rod-cone degeneration. Symptoms : Declining vision (at night and then in daylight) and eventual blindness. Age of onset : Between 2 and 12 years old. Frequency : Not available. Gene involved : PRCD. Tested mutation : c.5G>A. Transmission : Autosomal Recessive. Patent : _. Notes : _. PrintSend to a friendTweet WidgetPartager sur Facebook ...

An autosomal recessive rod-cone degeneration. This is a later onset condition, with earliest signs being seen at around 1.5-2 years of age. After this there is progressive loss of vision, and complete blindness will occur around 3-4 years later. The disease has been designated PRA-rdAc. This form of disease is more prevalent than the autosomal dominant form and is present in Abyssinian and Somali cats. The responsible gene has been identified and is designated CEP290 - DNA tests for cats are available. This defect now appears to be present in a wide range of different breeds, including: ...

Using cell transplants or stem cells to treat a retinal degenerative disease. Cell-Based Therapy (CBT) is one of the Foundations seven research priority areas. Scientists and clinicians are testing treatments for retinal degenerative diseases with stem cell and retinal transplants. This therapy has the potential to treat all retinal degenerative diseases, even in those people who have completely lost all photoreceptor and/or RPE cells.

Moderate aerobic exercise helps to preserve the structure and function of nerve cells in the retina after damage, according to an animal study appearing February 12 in The Journal of Neuroscience. The findings suggest exercise may be able to slow the progression of retinal degenerative diseases. Full Story →. ...

Progressive Retinal Atrophy, Progressive Rod-Cone Degeneration (PRA-prcd) is inherited as an autosomal recessive disease. Degeneration of both rod and cone photoreceptor cells of the retina of PRA-prcd affected dogs usually occurs 3 to 5 years of age or later. Affected dogs initially experience night blindness and loss of peripheral vision. As the disease progresses, complete blindness will occur in time. Different breeds and individual dogs may experience variation in the age and rate of the disease progression.. DDC Veterinary is offering DNA Testing for PRA-prcd (PRCD c.5G,A). Breeders have an accurate, convenient, and affordable tool to help them avoid producing PRA-prcd affected offspring and significantly reduce the gene frequency in future generations.. This mutation affects several breeds like the Chesapeake Bay Retriever, Chihuahua, Cocker Spaniel, Golden Retriever, Labrador Retriever, Poodle and Yorkshire Terrier. To see if this test is available for your breed, use the Order Canine ...

TY - JOUR. T1 - Effects of basic FGF on retinal degeneration in vitiligo (mivit/mivit) mice. AU - Smith, Sylvia B. AU - Titelman, R. M.. AU - Hamasaki, D. I.. PY - 1996/2/15. Y1 - 1996/2/15. N2 - Purpose: The growth factor, bFGF, slows the rate of photoreceptor cell (PRC) degeneration in the RCS rat, a model with defective RPE phagocytosis. The purpose of the present study was to determine whether bFGF could retard the rate of PRC loss in the vitiligo mouse, a model in which PRCs are lost slowly over many months. The cause of vitiligo PRC death is not known, but we have evidence that the RPE is the primary cellular site of the retinal defect: RPE microvillous processes are malformed in the optic nerve head region and phagocytosis of outer segment disks is reduced. Methods: bFGF [0.5μg/eye] was injected intravitreally into vitiligo mice at ages 2, 4, 6, 8 and 13 weeks; the contralateral eye served as vehicle control. Scotopic ERGs were performed on one group of mice prior to killing. Mice were ...

Dive into the research topics of Moderate Light-Induced Degeneration of Rod Photoreceptors with Delayed Transducin Translocation in shaker1 Mice. Together they form a unique fingerprint. ...

Progressive retinal atrophy (PRA) as an inherited disease occurs in many dog breeds and also in different forms. The form of progressive rod-cone degeneration (prcd-PRA) is a photoreceptor degeneration in dogs with varying ages of onset. This genetic disorder causes the degeneration of retinal cells in the eye: firstly, rod cells are affected, thus leading to progressive night blindness. Secondly, degeneration of the cone cells results in complete blindness of the dog, even in full light situations during the day. Age of onset of clinical symptoms is typically in early adolescence or early adulthood. However, the onset of the disease may vary among different dog breeds. Since diagnosis of retinal diseases in dogs may prove difficult, the genetic test on prcd-PRA helps to diagnose a specific disease and is also a useful tool for breeders to eliminate the mutated gene from the dog population. The mutation in the PRCD gene which has been suggested to cause prcd-PRA has recently been

TY - JOUR. T1 - Levels of retinoic acid and retinaldehyde dehydrogenase expression in eyes of the Mitf-vit mouse model of retinal degeneration.. AU - Duncan, T.. AU - Swint, C.. AU - Smith, S. B.. AU - Wiggert, B. N.. PY - 1999/6/28. Y1 - 1999/6/28. N2 - PURPOSE: Several reports have characterized the retinal degeneration observed in the Mitf(vit) mutant mouse. Despite these reports, the factor(s) that may cause or modulate the degeneration still are not well defined; however, it is known that the photoreceptors of Mitf(vit) mice die through an apoptotic mechanism. We reported previously that retinoid metabolism in the RPE of Mitf(vit)++ mice is perturbed. Retinoids regulate genes via the RAR and RXR nuclear receptor pathway that are involved in numerous cellular responses including apoptosis. It is possible that retinoic acid (RA) modulates the retinal degeneration observed in the Mitf(vit) mice. The purpose of this study was to evaluate the levels of RA in whole eyes, as well as its ...

Light exposure induces oxidative stress, which contributes to ocular diseases of aging. Blue light provides a model for light-induced oxidative stress, lipid peroxidation and retinal degeneration in Drosophila melanogaster. In contrast to mature adults, which undergo retinal degeneration when exposed to prolonged blue light, newly-eclosed flies are resistant to blue light-induced retinal degeneration. Here, we sought to characterize the gene expression programs induced by blue light in flies of different ages to identify neuroprotective pathways utilized by photoreceptors to cope with light-induced oxidative stress. To identify gene expression changes induced by blue light exposure, we profiled the nuclear transcriptome of Drosophila photoreceptors from one- and six-day-old flies exposed to blue light and compared these with dark controls. Flies were exposed to 3 h blue light, which increases levels of reactive oxygen species but does not cause retinal degeneration. We identified substantial gene

Mutations in genes traditionally associated with syndromic retinal disease are increasingly found to cause nonsyndromic inherited retinal degenerations. Mutations in CLN3 are classically associated with juvenile neuronal ceroid lipofuscinosis, a rare neurodegenerative disease with early retinal degeneration and progressive neurologic deterioration, but have recently also been identified in patients with nonsyndromic inherited retinal degenerations. To our knowledge, detailed clinical characterization of such cases has yet to be reported.To provide detailed clinical, electrophysiologic, structural, and molecular genetic findings in nonsyndromic inherited retinal degenerations associated with CLN3 mutations.A multi-institutional case series of 10 patients who presented with isolated nonsyndromic retinal disease and mutations in CLN3. Patient ages ranged from 16 to 70 years; duration of follow-up ranged from 3 to 29 years.Longitudinal clinical evaluation, including full ophthalmic examination, ...

Combinations of Food and Drug Administration-approved drugs protect against the loss of cells required for vision in a mouse model of blinding retinal diseases. The study, published in Science Signaling, was funded by the National Eye Institute, a part of the National Institutes of Health.

Nephronophthisis (NPHP) is an autosomal recessive kidney disease that is often associated with vision and/or brain defects. To date, 11 genes are known to cause NPHP. The gene products, while structurally unrelated, all localize to cilia or centrosomes. Although mouse models of NPHP are available for 9 of the 11 genes, none has been described for nephronophthisis 4 (Nphp4). Here we report a novel, chemically induced mutant, nmf192, that bears a nonsense mutation in exon 4 of Nphp4. Homozygous mutant Nphp4nmf192/nmf192 mice do not exhibit renal defects, phenotypes observed in human patients bearing mutations in NPHP4, but they do develop severe photoreceptor degeneration and extinguished rod and cone ERG responses by 9 weeks of age. Photoreceptor outer segments (OS) fail to develop properly, and some OS markers mislocalize to the inner segments and outer nuclear layer in the Nphp4nmf192/nmf192 mutant retina. Despite NPHP4 localization to the transition zone in the connecting cilia (CC), the CC ...

Description: Progressive retinal atrophy is an inherited disease that occurs in many dog breeds and manifests itself in various forms. The form of a progressive rod and cone degeneration is photoreceptor degeneration and occurs at different dog ages. The genetic disorder causes the degeneration of retinal cells in the eye. The rods are first affected; therefore, night blindness occurs first. Consequently, the cones are impairment, resulting in the complete blindness of the animals in optimal lighting conditions, such as daylight. However, the time of onset may vary and depends on the breed of the dog from 2 to 12 years.. Inheritance: autosomal recessive. Mutation: c.5G,A in PRCD gene (previous designation 1298G,A). Sample: EDTA whole blood (1.0 ml) or 2 buccal brushes. For official purposes, the confirmation of the dogs identity by Veterinarian is recommended.. The analysis is suitable for the following breeds: American Eskimo Dog, Australian Cattle Dog, Australian Shepherd, Australian Shepherd ...

Aging causes anatomical and functional changes in visual and circadian systems. In wild type mice rods, cones, and photosensitive retinal ganglion cells (pRGCs) decline with age. In rd/rd cl mice, the early loss of rods and cones is followed by protracted transneuronal loss of inner retinal neurons as well as the pRGCs. Here we use Fos induction to study the light input pathway to the suprachiasmatic nuclei (SCN), the intergeniculate leaflets (IGL) and ventral lateral geniculate nuclei (vLGN) of old (~700 days) and young (~150 days) wild type and rd/rd cl mice. Cholera toxin tracing was used in parallel to study the anatomy of this pathway. We find that aging rather than retinal degeneration is a more important factor in reducing light input to the SCN, causing both a reduction in Fos expression and retinal afferents. Furthermore, we show light-induced Fos within the vLGN and IGL is predominantly subserved by rods and cones, and once again aging reduces the amplitude of this response. © 2012 Elsevier

Aging causes anatomical and functional changes in visual and circadian systems. In wild type mice rods, cones, and photosensitive retinal ganglion cells (pRGCs) decline with age. In rd/rd cl mice, the early loss of rods and cones is followed by protracted transneuronal loss of inner retinal neurons as well as the pRGCs. Here we use Fos induction to study the light input pathway to the suprachiasmatic nuclei (SCN), the intergeniculate leaflets (IGL) and ventral lateral geniculate nuclei (vLGN) of old (∼700 days) and young (∼150 days) wild type and rd/rd cl mice. Cholera toxin tracing was used in parallel to study the anatomy of this pathway. We find that aging rather than retinal degeneration is a more important factor in reducing light input to the SCN, causing both a reduction in Fos expression and retinal afferents. Furthermore, we show light-induced Fos within the vLGN and IGL is predominantly subserved by rods and cones, and once again aging reduces the amplitude of this response.

Our findings firmly establish that increased expression of PR STAT3 and pSTAT3Tyr705 has a prosurvival role in mutant PRs. First, we found that endogenous Stat3 expression was significantly increased in the mutant PRs from two unrelated IPD models, Tg(RHO P347S) and Prph2rds/+ mice. Second, deletion of Stat3 in mutant PRs greatly increased the degree of PR death. Third, augmentation of either STAT3wt or STAT3C expression, using R26 transgenes, significantly enhanced mutant PR survival in both Tg(RHO P347S) and Prph2rds/+ mice and improved retinal electrophysiology in the one model tested [Tg(RHO P347S)]. Taken together, these results suggest a cell-autonomous protective role for STAT3 in mutant PRs. The role of the Müller cell Stat3 activation in IPDs is unknown. Our findings, together with other work suggesting that increased pSTAT3Tyr705 expression may be protective against a variety of neuronal insults (41⇓-43), indicate that enhanced Stat3 signaling merits study as a general ...

We describe, in detail, the phenotype of late-onset retinal macular degeneration (L-ORMD) an inherited condition affecting both the retina and anterior segment. We propose a staging based on clinical characteristics and discuss the relevance of this condition to our understanding of age-related macular degeneration.. Methods: A systematic review of the literature regarding this condition support a detailed description of the natural history. Clinical experiences in identifying, monitoring and managing patients are also presented.. Results: L-ORMD is a rare fully penetrant autosomal dominant condition resulting from a mutation (Ser163Arg) in chromosome 11q. Affected individuals develop bilateral loss of vision, dark adaptation abnormalities, fundus drusen like yellow spots, mid peripheral pigmentation, choroidal neovascularisation, retinal atrophy and long anteriorly inserted lens zonules. Patients may benefit from treatment with high dose vitamin A.. Conclusions: Raised awareness of L-ORMD ...

Misregulation of the innate immune response and other immune-related processes have been suggested to play a critical role in the pathogenesis of a number of different neurodegenerative diseases, including age related macular degeneration. In an animal model for photoreceptor degeneration, several genes of the innate and acquired immune system were found to be differentially regulated in the retina during the degenerative process. In addition to this differential regulation of individual genes, we found that in the rd1 retina a significantly higher number of genes involved in immune-related responses were expressed at any given time during the degenerative period. The peak of immune-related gene expression was at postnatal day 14, coinciding with the peak of photoreceptor apoptosis in the rd1 mouse. We directly tested the potential involvement of acquired and innate immune responses in initiation and progression of photoreceptor degeneration by analyzing double mutant animals. Retinal morphology ...

The Metabolic Response of Müller Glial Cells to Photoreceptor Degeneration. F.R. Vazquez-Chona, W.D. Ferrell, B.W. Jones, R.E. Marc. Ophthalmology, Moran Eye Center, Univ. of Utah, Salt Lake City, UT. ARVO 2010.. Roles of Retinoic Acid Signalling in Neuritogenesis During Light-Induced Retinal Degeneration. Y-H. Lin, B.W. Jones, K. Rapp, M.V. Shaw, J-H. Yang, C.B. Watt, R.E. Marc. Ophthalmology, Moran Eye Center, Univ. of Utah, Salt Lake City, UT. ARVO 2010.. Retinal Progenitor Sheet Transplants to Rats With Retinal Degeneration - Circuitry Between Transplant and Host. M.J. Seiler1A,1B, B.W. Jones2, R.B. Aramant1A, R.E. Marc2, H.S. Keirstead1A,1B. AAnatomy & Neurobiol/Reeve-Irvine Res Ctr, BSue & Bill Gross Stem Cell Research Center, 1UC Irvine, Irvine, CA; 2Ophthalmology, Moran Eye Center, Univ. of Utah, Salt Lake City, UT. 13th International Meeting on Neural Regeneration. Ultrastructural Mapping of Neural Circuity, A Computational Framework J.R. Anderson1, B. W. Jones1, J-H Yang1, M.V. Shaw1, ...

I just learned this afternoon, of a start-up company, MitoChem Therapeutics, which is apparently an outgrowth of the Vision Research program at the Ophthalmology department at the University of South Carolina. Two of their scientists, Drs. Rohrer and Beeson, have been looking into compounds that can provide energy to reduced capacity mitochondria in retinal cells that are possibly at the root of retinal degenerations in such diseases as retinitis pigmentosa and macular degeneration. ...

Within the family of retinal degenerations there are multiple known diseases which differ in their pathology, prognosis and visual symptoms. It is difficult to predict the extent of vision loss or how fast the disease might progress but in many cases people with retinal degenerative disease will eventually suffer complete vision loss. Eye disease treatment with stem cells is showing remarkable results in increasing the vision of our patients.. Over 200 million people worldwide suffer from blindness or low vision due to a variety of diseases, including retinal degenerative disease. The two most prevalent retinal degenerative diseases are - Age-related Macular Degeneration primarily affecting people age 60 and older, and Retinitis Pigmentosa which is the most common inherited cause of blindness in people between the ages of 20 and 60 worldwide4.. Age Related Macular Degeneration (AMD) afflicts an estimated 170 million worldwide. Since AMD develops with age, with a growing aging population the ...

Monai et al characterized the longitudinal retinal degeneration of a rat model of retinitis pigmentosa using the Phoenix Micron OCT to examine retinal layers in live rats and the full field Ganzfeld ERG to test function. The rats have one of the mutations, P23H, that cause retinitis pigmentosa in humans, and are specifically a very. ...

Inherited retinal degenerations afflict 1 in 3,500 individuals and are a heterogeneous group of diseases that result in profound vision loss, usually the result of retinal neuronal apoptosis. Atrophic changes in the retinal vasculature are also observed in many of these degenerations. While it is thought that this atrophy is secondary to diminished metabolic demand in the face of retinal degeneration, the precise relationship between the retinal neuronal and vascular degeneration is not clear. In this study we demonstrate that whenever a fraction of mouse or human adult bone marrow-derived stem cells (lineage-negative hematopoietic stem cells [Lin- HSCs]) containing endothelial precursors stabilizes and rescues retinal blood vessels that would ordinarily completely degenerate, a dramatic neurotrophic rescue effect is also observed. Retinal nuclear layers are preserved in 2 mouse models of retinal degeneration, rd1 and rd10, and detectable, albeit severely abnormal, electroretinogram recordings ...

The Retinal Degeneration Center was established in 1990 by the University of Michigan to emphasize research into retinal diseases that cause progressive vision loss. To date, over 140 different genetic diseases have been identified that cause visual loss, either centrally or peripherally.

Optical coherence tomography (OCT) is a novel method of retinal in vivo imaging. In this study, we assessed the potential of OCT to yield histology-analogue sections in mouse models of retinal degeneration. We achieved to adapt a commercial 3(rd) generation OCT system to obtain and quantify high-resolution morphological sections of the mouse retina which so far required in vitro histology. OCT and histology were compared in models with developmental defects, light damage, and inherited retinal degenerations. In conditional knockout mice deficient in retinal retinoblastoma protein Rb, the gradient of Cre expression from center to periphery, leading to a gradual reduction of retinal thickness, was clearly visible and well topographically quantifiable. In Nrl knockout mice, the layer involvement in the formation of rosette-like structures was similarly clear as in histology. OCT examination of focal light damage, well demarcated by the autofluorescence pattern, revealed a practically complete loss ...

This gene encodes a microtubule-binding nuclear protein that localizes to the centrioles of dividing cells and differentiating multiciliated cells and negatively regulates centriole duplication. The encoded protein is closely associated with the centriole barrel, and resides in the centriole lumen. Naturally-occurring mutations in the orthologous mouse gene are associated with age-related retinal degeneration. [provided by RefSeq, Feb 2019 ...

Only proceedings of a very prestigious conference A comprehensive source for the latest basic research in the field of retinal degenerative diseases

Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies characterized by progressive and irreversible loss of vision due to rod and cone degeneration. Evidence suggests that an inappropriate oxygen level could contribute to its pathogenesis. Rod cell death could increase oxygen concentration, reduce hypoxia-inducible factor 1 (HIF-1α) and contribute to cone cell death. The purposes of this study were: 1) to analyze the temporal profile of HIF-1α, its downstream effectors VEGF, endothelin-1 (ET-1), iNOS, and glucose transporter 1 (GLUT1), and neuroinflammation in retinas of the murine model of rd10 (retinal degeneration 10) mice with RP; 2) to study oxygen bioavailability in these retinas; and 3) to investigate how stabilizing HIF-1α proteins with dimethyloxaloglycine (DMOG), a prolyl hydroxylase inhibitor, affects retinal degeneration, neuroinflammation, and antioxidant response in rd10 mice ...

Rakoczy, P. E., Lai, C. M., Yu, M. J. T., Daniels, D. M., Brankov, M., Rae, B. C., Stoddart, C. W., Barnett, N. L., Martin-Iverson, M. T., Redmond, T. M., Narfstrom, K., Zhou, X. & Constable, I. J., 1 Dec 2003, Retinal Degenerations: Mechanisms and Experimental Therapy: Proceedings of the X International Symposium on Retinal Degeneration, held September 30-0ctober 5, 2002, in Burgenstock, Switzerland . LaVail, M. M., Hollyfield, J. G. & Anderson, R. E. (eds.). Boston: Springer, p. 431-438 8 p. (Advances in Experimental Medicine and Biology; vol. 533).. Research output: Chapter in Book/Report/Conference proceeding › Conference contribution › Research › peer-review ...

Table 1. Quantitative trait loci. Table shows the LRS, LOD score, percent effect, percent genetic effect, inheritance pattern, and which allele is protective against constant light-induced retinal damage for the quantitative trait loci (QTL) detected in this constant light-induced retinal degeneration intercross study between NZW/LacJ and C57BL/6J-c2J. In the Significance (Sig) column, HS represents highly significant, S represents significant, and Sugg represents suggestive, NS represents not significant. CentiMorgan (cM) positions are the distances from the centromere taken from linkage maps at the MGI web site (JAX). Megabase (Mb) positions were determined from the MGSCv3 sequence database and rounded to the nearest 0.1 million bases from the centromere. The - percentage genetic effect score indicates an NZW protective allele; all other percentage genetic effect scores indicate B6al protective alleles.. ...

This is a great review paper on the role of rhodopsin trafficking and its influence on retinal degenerative disease by TJ Hollingsworth and Alecia Gross. Rhodopsin delocalization in rod photoreceptors has been recognized for some time as one of the first indications of retinal photoreceptor cell stress in retinal degenerative diseases, so I was intrigued when seeing this paper come up in PubMed. Continue reading Review: Defective Trafficking of Rhodopsin and Its Role In Retinal Degenerations. ...

Retinal degeneration is mostly a hereditary disease that is characterized by the death of photoreceptors - the light-sensitive neurons in the eye - which eventually leads to blindness. While many have attempted to treat the disease through retinal transplants, and some have shown that transplanting graft photoreceptors to the host without substantial integration can rescue retinal function, until now, no one has conclusively succeeded in transplanting photoreceptors that functionally connect to host cells and send visual signals to the host retina and brain. The researchers studied this problem using a mouse model for end-stage retinal degeneration in which the outer nuclear layer of the retina is completely missing. This is an important issue because in clinical practice this type of therapy would most likely target end-stage retinas in which of the photoreceptors are dead and the next neurons up the chain do not have any input. Researchers have recently shown that 3D retinal sheets derived ...

Inherited retinal degenerations (IRDs) are important causes of vision loss that affect people of all ages. These disorders cause vision loss via dysfunction and death of the photoreceptor and retinal pigment epithelial cells of the retina. Gene augmentation therapy has been shown to be beneficial for patients with specific genetic forms of IRDs to date, but IRDs are genetically heterogeneous, and gene therapy may not be possible for all of the different genetic forms of disease, such as those caused by mutations in large genes, or by dominant gain-of-function mutations. This project is to test the use of CRISPR/Cas9 - mediated genome editing to treat several genetic forms of retinal degeneration that are not amenable to standard gene augmentation therapy approaches. The role of the defined student will be to learn and apply skills in genetics, molecular and cellular biologic, and CRISPR/Cas9 genome editing for treating one of the dominant forms of IRD in patient-derived iPS cells and gene ...

Experimental animals. Experiments were performed using Wistar rats, C57BL/6J mice, and p75NTR knock-out mice (purchased from the Jackson Laboratory) in accordance with the ARVO statement for the Use of Animals in Vision Research. Animals were maintained in either a 12 hr light/dark cycle (LD 12:12) or 24 hr of constant illumination. Light intensity inside the cages ranged from 100 to 200 lux under LD 12:12, whereas 800-1300 lux was used for 24 hr of constant illumination to effect light-induced retinal degeneration (Harada et al., 1996, 1998a).. Immunohistochemistry. Rats were anesthetized with diethylether and perfused transcardially with saline, followed by 4% paraformaldehyde in 0.1 m phosphate buffer containing 0.5% picric acid at room temperature. Rat eyes were removed and postfixed overnight in the same fixative and then embedded in paraffin. The posterior portion of the eye was sectioned sagittally at 7 μm thickness, mounted, and stained with hematoxylin and eosin. For ...

Weve published a new paper, another review on retinal remodeling in JJO (pdf here) that describes what happens in retinal degenerations. Authors are myself, Mineo Kondo, Hiroko Terasaki, Yanhua Lin, Maureen McCall and Robert E. Marc.. Ill use this paper to bootstrap an upcoming talk on retinal remodeling in Berlin and a chapter in Webvision.. Borrowing from the abstract… Retinal remodeling is a universal finding subsequent to retinal degenerative disease that results in deafferentation of the neural retina from photoreceptor input as downstream neuronal elements respond to loss of input with negative plasticity. This negative plasticity is not passive in the face of photoreceptor degeneration, with a phased revision of retinal structure and function found at the molecular, synaptic, cell, and tissue levels involving all cell classes in the retina, including neurons and glia. Retinal remodeling has direct implications for the rescue of vision loss through bionic or biological approaches, as ...

The research focus of my group is on photoreceptor metabolism and the signaling pathways that regulate photoreceptor metabolism. We study retinal degenerative diseases that affect cone photoreceptors, since cones are essential for color, daylight and high acuity vision in humans. - Age-related macular degeneration (AMD) is one of the leading causes for blindness in the industrialized world. - Retinitis Pigmentosa is an inherited retinal degenerative disease that leads to blindness. - mTORC1 - Insulin - rod-cone distrophy - Punzo Lab UMass Worcester

Unfortunately, these same mechanisms, if not regulated properly, can be harmful to us. It turns out that these powerful molecules are also involved in the death of retinal cells in age-related macular degeneration (AMD).. Last week, 150 retinal scientists from around the world met in Bad Goegging, Germany, for the 15th International Symposium on Retinal Degenerations to discuss a variety of research efforts and advances, and the role of the complement system was a major topic of discussion. Many of the talks focused on how we can use natural complement control mechanisms in the body to stop the damage.. In addition, there were several discussions on how to better determine the actual genetic risk for getting AMD, and how high-risk, complement-related genes affect someones response to Lucentis, Avastin or Eylea, the current treatments available for wet AMD.. It was in 2005 that Foundation-funded researchers first discovered that genes associated with the complement system were linked to AMD. The ...

Scientists have successfully transplanted light-sensing cells called p...The achievement is based on a novel technology in which the cells are ...The team of scientists found that transplanted photoreceptor precursor...Rather than injecting undifferentiated and uncommitted stem cells into...The findings reported in the November 9 advance online issue of Natur...,Transplanted,photoreceptor,precursor,cells,restore,visual,function,in,mice,with,retinal,degeneration,biological,biology news articles,biology news today,latest biology news,current biology news,biology newsletters

Physicians in the Retina & Uveitis Service at the Kellogg Eye Center have extensive experience in the treatment of diseases and conditions such as retinal detachment, diabetic retinopathy, retinitis pigmentosa, vascular occlusive disease, age-related macular degeneration, macular holes, hereditary retinal degenerations, ocular inflammation, and ocular tumors.

In the human disease retinitis pigmentosa the photoreceptors degenerate, leading to blindness. Electrical prostheses can elicit visual sensations in patients; however, processes secondary to photoreceptor death lead to pathological rhythmic activity in the remaining retinal network that seems to interfere with this therapeutic approach. We study and characterize signal transmission in both healthy and diseased mouse retina and, in co-operation with partners from universities and from within the Forschungszentrum, aim at developing improved prosthetic devices ...