ReviewOrphanet journal of rare diseases2007
Cone rod dystrophies.
Review in Orphanet journal of rare diseases, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 227 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
227 citing papers in PubMed, 1 synthesis or guideline pooled it, 438 citations in OpenAlex.
- A systematic review of inherited retinal dystrophies in Pakistan: updates from 1999 to April 2023.BMC ophthalmology · 2024Pooled it
- Multiexon deletion alleles of ATF6 linked to achromatopsia.JCI insight · 2020Trial
- Identification of Novel Mutations in ABCA4 Gene: Clinical and Genetic Analysis of Indian Patients with Stargardt Disease.BioMed research international · 2015Trial
- Clinical and Population-Specific Insights Into Inherited Retinal Dystrophies From Whole-Exome Sequencing of the Polish Cohort.Investigative ophthalmology & visual science · 2026Article
- Identification of a Duplication in the RP17 Locus in an Individual With Pathogenic CEP290 Variants: Implications for RP17 Variant Classification.Investigative ophthalmology & visual science · 2026Article
- Visualising treatment effects in low-vision settings: proven and potential endpoints for clinical trials of inherited retinal disease therapies.Gene therapy · 2026Review
- Sporadic cone-rod dystrophy caused by a heterozygous RAB28 p.Ser23Phe pathogenic variant and a de novo 4p16.1p15.33 deletion.BMC medical genomics · 2026Article
- Ciliary Defects in Inherited Retinal Diseases.Advanced genetics (Hoboken, N.J.) · 2026Review
- Case series: The value of fundus autofluorescence in inherited macular disease.Optometry and vision science : official publication of the American Academy of Optometry · 2026Article
- Article
- Syntaxin 3B Mediates Light-Dependent Interactions with STXBP1 and Arrestin 4: Distinct Roles in Rods and Cones.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Dysfunction of Unc119, a Transducin-Binding Protein, Leads to Cone-Rod Dystrophy through Activating JAK-Stat and NF-κB Inflammatory Pathways in the Mouse Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Article
- Multidimensional Quantification of Macular Cone Activity in Pattern Electroretinography Using Discrete Wavelet Transform.Translational vision science & technology · 2025Article
- Safety and efficacy of MCO-010 optogenetic therapy in patients with Stargardt disease in USA (STARLIGHT): an open-label multi-center Ph2 trial.EClinicalMedicine · 2025Article
- A Comprehensive Review of Congenital Eye Diseases in Pediatrics: Etiology, Diagnosis, and Management.Cureus · 2025Review
- Novel splice variants implicated in inherited retinal dystrophies in two Moroccan families.Molecular biology reports · 2025Article
- Novel compound heterozygousExperimental and therapeutic medicine · 2025Article
- "My child can't see"-workup and management of children with low vision: a joint workshop of the AAPOS Low Vision Rehabilitation and Genetic Eye Diseases Committees.Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus · 2025Review
167 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cone rod dystrophies (CRDs) (prevalence 1/40,000) are inherited retinal dystrophies that belong to the group of pigmentary retinopathies. CRDs are characterized by retinal pigment deposits visible on fundus examination, predominantly localized to the macular region. In contrast to typical retinitis pigmentosa (RP), also called the rod cone dystrophies (RCDs) resulting from the primary loss in rod photoreceptors and later followed by the secondary loss in cone photoreceptors, CRDs reflect the opposite sequence of events. CRD is characterized by primary cone involvement, or, sometimes, by concomitant loss of both cones and rods that explains the predominant symptoms of CRDs: decreased visual acuity, color vision defects, photoaversion and decreased sensitivity in the central visual field, later followed by progressive loss in peripheral vision and night blindness. The clinical course of CRDs is generally more severe and rapid than that of RCDs, leading to earlier legal blindness and disability. At end stage, however, CRDs do not differ from RCDs. CRDs are most frequently non syndromic, but they may also be part of several syndromes, such as Bardet Biedl syndrome and Spinocerebellar Ataxia Type 7 (SCA7). Non syndromic CRDs are genetically heterogeneous (ten cloned genes and three loci have been identified so far). The four major causative genes involved in the pathogenesis of CRDs are ABCA4 (which causes Stargardt disease and also 30 to 60% of autosomal recessive CRDs), CRX and GUCY2D (which are responsible for many reported cases of autosomal dominant CRDs), and RPGR (which causes about 2/3 of X-linked RP and also an undetermined percentage of X-linked CRDs). It is likely that highly deleterious mutations in genes that otherwise cause RP or macular dystrophy may also lead to CRDs. The diagnosis of CRDs is based on clinical history, fundus examination and electroretinogram. Molecular diagnosis can be made for some genes, genetic counseling is always advised. Currently, there is no therapy that stops the evolution of the disease or restores the vision, and the visual prognosis is poor. Management aims at slowing down the degenerative process, treating the complications and helping patients to cope with the social and psychological impact of blindness.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.