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Article ; Online: Inherited Optic Neuropathies: Real-World Experience in the Paediatric Neuro-Ophthalmology Clinic.

Gilhooley, Michael James / Raoof, Naz / Yu-Wai-Man, Patrick / Moosajee, Mariya

2024 Volume 15, Issue 2

Abstract: Inherited optic neuropathies affect around 1 in 10,000 people in England; in these conditions, vision is lost as retinal ganglion cells lose function or die (usually due to pathological variants in genes concerned with mitochondrial function). Emerging ... ...

Abstract	Inherited optic neuropathies affect around 1 in 10,000 people in England; in these conditions, vision is lost as retinal ganglion cells lose function or die (usually due to pathological variants in genes concerned with mitochondrial function). Emerging gene therapies for these conditions have emphasised the importance of early and expedient molecular diagnoses, particularly in the paediatric population. Here, we report our real-world clinical experience of such a population, exploring which children presented with the condition, how they were investigated and the time taken for a molecular diagnosis to be reached. A retrospective case-note review of paediatric inherited optic neuropathy patients (0-16 years) in the tertiary neuro-ophthalmology service at Moorfields Eye Hospital between 2016 and 2020 identified 19 patients. Their mean age was 9.3 ± 4.6 (mean ± SD) years at presentation; 68% were male, and 32% were female; and 26% had comorbidities, with diversity of ethnicity. Most patients had undergone genetic testing (95% (
MeSH term(s)	Humans ; Male ; Female ; Child ; Child, Preschool ; Adolescent ; Optic Atrophy, Hereditary, Leber/genetics ; Optic Atrophy, Autosomal Dominant/genetics ; Retrospective Studies ; Ophthalmology ; Optic Nerve Diseases/diagnosis ; Optic Nerve Diseases/genetics ; Optic Nerve Diseases/therapy
Language	English
Publishing date	2024-01-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes15020188
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Article ; Online: Psychometric Validity of the Visual Function Index in Leber Hereditary Optic Neuropathy.

Chen, Benson S / Yu-Wai-Man, Patrick / Horton, Mike

Translational vision science & technology

2023 Volume 12, Issue 1, Page(s) 23

Abstract: Purpose: The purpose of this study was to determine the psychometric validity of the Visual Function Index (VF-14) for use by patients with Leber hereditary optic neuropathy (LHON).: Methods: Rasch analysis was conducted in two stages using data for ... ...

Abstract	Purpose: The purpose of this study was to determine the psychometric validity of the Visual Function Index (VF-14) for use by patients with Leber hereditary optic neuropathy (LHON). Methods: Rasch analysis was conducted in two stages using data for 196 individuals (74.5% male) carrying one of the three primary LHON mutations and affected by vision loss. In stage 1, scale unidimensionality, scale-to-sample targeting, response category threshold ordering, item fit statistics, local dependency, and reliability were assessed. In stage 2, iterative post-hoc revisions of the VF-14 structure (VF-14R) were applied and psychometrically re-evaluated. Results: Issues identified with the VF-14 included disordered response thresholds (12/14 items), local dependency (10/91 pairwise dependencies), and evidence of multidimensionality. However, the distribution of person estimates and item thresholds were fairly well matched, only one item showed misfit to the Rasch model, and there was good reliability (Person Separation Index 0.84). Rasch-informed VF-14 revisions included removing both driving items and the misfitting sports item, rescoring response options across all items by merging two response categories, and accounting for the dependency between two reading items. The VF-14R demonstrated improved psychometric validity. Conclusions: Clinicians and researchers using the VF-14 with LHON patients should be aware of its limitations. Compared to the original version, the proposed Rasch-based structure of the VF-14R appears to offer improved psychometric performance and interpretation of vision-related activity limitation. Translational relevance: The original version of the VF-14 exhibits several limitations that undermines its psychometric validity as a patient-reported outcome measure for patients with LHON.
MeSH term(s)	Humans ; Male ; Female ; Psychometrics ; Optic Atrophy, Hereditary, Leber/diagnosis ; Optic Atrophy, Hereditary, Leber/genetics ; Reproducibility of Results ; Vision, Ocular ; Blindness
Language	English
Publishing date	2023-01-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2674602-5
ISSN	2164-2591 ; 2164-2591
ISSN (online)	2164-2591
ISSN	2164-2591
DOI	10.1167/tvst.12.1.23
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Article ; Online: Blurred Disc Margins.

Britton, John O T / Yu-Wai-Man, Patrick / Chen, Benson S

Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society

2023 Volume 43, Issue 2, Page(s) e63

MeSH term(s)	Humans ; Papilledema ; Optic Disk/diagnostic imaging
Language	English
Publishing date	2023-04-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	1189901-3
ISSN	1536-5166 ; 1070-8022
ISSN (online)	1536-5166
ISSN	1070-8022
DOI	10.1097/WNO.0000000000001842
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Article: Mitochondrial optic neuropathies.

Carelli, Valerio / La Morgia, Chiara / Yu-Wai-Man, Patrick

Handbook of clinical neurology

2023 Volume 194, Page(s) 23–42

Abstract: Mitochondrial optic neuropathies have a leading role in the field of mitochondrial medicine ever since 1988, when the first mutation in mitochondrial DNA was associated with Leber's hereditary optic neuropathy (LHON). Autosomal dominant optic atrophy ( ... ...

Abstract	Mitochondrial optic neuropathies have a leading role in the field of mitochondrial medicine ever since 1988, when the first mutation in mitochondrial DNA was associated with Leber's hereditary optic neuropathy (LHON). Autosomal dominant optic atrophy (DOA) was subsequently associated in 2000 with mutations in the nuclear DNA affecting the OPA1 gene. LHON and DOA are both characterized by selective neurodegeneration of retinal ganglion cells (RGCs) triggered by mitochondrial dysfunction. This is centered on respiratory complex I impairment in LHON and defective mitochondrial dynamics in OPA1-related DOA, leading to distinct clinical phenotypes. LHON is a subacute, rapid, severe loss of central vision involving both eyes within weeks or months, with age of onset between 15 and 35 years old. DOA is a more slowly progressive optic neuropathy, usually apparent in early childhood. LHON is characterized by marked incomplete penetrance and a clear male predilection. The introduction of next-generation sequencing has greatly expanded the genetic causes for other rare forms of mitochondrial optic neuropathies, including recessive and X-linked, further emphasizing the exquisite sensitivity of RGCs to compromised mitochondrial function. All forms of mitochondrial optic neuropathies, including LHON and DOA, can manifest either as pure optic atrophy or as a more severe multisystemic syndrome. Mitochondrial optic neuropathies are currently at the forefront of a number of therapeutic programs, including gene therapy, with idebenone being the only approved drug for a mitochondrial disorder.
MeSH term(s)	Child, Preschool ; Male ; Humans ; Optic Nerve Diseases ; Optic Atrophy, Hereditary, Leber/genetics ; Optic Atrophy, Hereditary, Leber/therapy ; Mitochondrial Diseases/genetics ; Mitochondria/genetics ; DNA, Mitochondrial/genetics ; Optic Atrophy, Autosomal Dominant/genetics ; Optic Atrophy, Autosomal Dominant/therapy ; Mutation
Chemical Substances	DNA, Mitochondrial
Language	English
Publishing date	2023-02-20
Publishing country	Netherlands
Document type	Review ; Journal Article
ISSN	0072-9752
ISSN	0072-9752
DOI	10.1016/B978-0-12-821751-1.00010-5
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Article ; Online: From Bench to Bedside-Delivering Gene Therapy for Leber Hereditary Optic Neuropathy.

Chen, Benson S / Yu-Wai-Man, Patrick

Cold Spring Harbor perspectives in medicine

2022 Volume 12, Issue 6

Abstract: Leber hereditary optic neuropathy (LHON) is a rare, maternally inherited mitochondrial disorder that presents with severe bilateral sequential vision loss, due to the selective degeneration of retinal ganglion cells (RGCs). Since the mitochondrial ... ...

Abstract	Leber hereditary optic neuropathy (LHON) is a rare, maternally inherited mitochondrial disorder that presents with severe bilateral sequential vision loss, due to the selective degeneration of retinal ganglion cells (RGCs). Since the mitochondrial genetic basis for LHON was uncovered in 1988, considerable progress has been made in understanding the pathogenetic mechanisms driving RGC loss, which has enabled the development of therapeutic approaches aimed at mitigating the underlying mitochondrial dysfunction. In this review, we explore the genetics of LHON, from bench to bedside, focusing on the pathogenetic mechanisms and how these have informed the development of different gene therapy approaches, in particular the technique of allotopic expression with adeno-associated viral vectors. Finally, we provide an overview of the recent gene therapy clinical trials and consider the unanswered questions, challenges, and future prospects.
MeSH term(s)	DNA, Mitochondrial/genetics ; Genetic Therapy/methods ; Humans ; Optic Atrophy, Hereditary, Leber/genetics ; Optic Atrophy, Hereditary, Leber/pathology ; Optic Atrophy, Hereditary, Leber/therapy ; Retinal Ganglion Cells/pathology
Chemical Substances	DNA, Mitochondrial
Language	English
Publishing date	2022-07-21
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a041282
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Article ; Online: Mitochondria and the eye-manifestations of mitochondrial diseases and their management.

Chen, Benson S / Harvey, Joshua P / Gilhooley, Michael J / Jurkute, Neringa / Yu-Wai-Man, Patrick

Eye (London, England)

2023 Volume 37, Issue 12, Page(s) 2416–2425

Abstract: Historically, distinct mitochondrial syndromes were recognised clinically by their ocular features. Due to their predilection for metabolically active tissue, mitochondrial diseases frequently involve the eye, resulting in a range of ophthalmic ... ...

Abstract	Historically, distinct mitochondrial syndromes were recognised clinically by their ocular features. Due to their predilection for metabolically active tissue, mitochondrial diseases frequently involve the eye, resulting in a range of ophthalmic manifestations including progressive external ophthalmoplegia, retinopathy and optic neuropathy, as well as deficiencies of the retrochiasmal visual pathway. With the wider availability of genetic testing in clinical practice, it is now recognised that genotype-phenotype correlations in mitochondrial diseases can be imprecise: many classic syndromes can be associated with multiple genes and genetic variants, and the same genetic variant can have multiple clinical presentations, including subclinical ophthalmic manifestations in individuals who are otherwise asymptomatic. Previously considered rare diseases with no effective treatments, considerable progress has been made in our understanding of mitochondrial diseases with new therapies emerging, in particular, gene therapy for inherited optic neuropathies.
MeSH term(s)	Humans ; Syndrome ; Mitochondrial Diseases/diagnosis ; Mitochondrial Diseases/genetics ; Mitochondrial Diseases/therapy ; Mitochondria/genetics ; Mitochondria/metabolism ; Optic Nerve Diseases/complications ; Retinal Diseases/complications
Language	English
Publishing date	2023-04-25
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	91001-6
ISSN	1476-5454 ; 0950-222X
ISSN (online)	1476-5454
ISSN	0950-222X
DOI	10.1038/s41433-023-02523-x
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Article ; Online: Neuroimaging changes in the pregeniculate visual pathway and chiasmal enlargement in Leber hereditary optic neuropathy.

Xu, Xintong / Zhou, Huanfen / Sun, Mingming / Li, Yuyu / Chen, Biyue / Chen, Xiyun / Xu, Quangang / Yu-Wai-Man, Patrick / Wei, Shihui

The British journal of ophthalmology

2024

Abstract: ... groups (p=0.039). Furthermore, significantly more patients in the m.11778G>A group (16 patients (57 ... p=0.005). Optic chiasmal enlargement was more common in patients with vision loss duration <3 months ... compared with those ≥3 months (p=0.028).: Conclusion: T2 HS in the pregeniculate visual pathway is ...

Abstract	Purpose: To describe the pattern of MRI changes in the pregeniculate visual pathway in Leber hereditary optic neuropathy (LHON). Method: This retrospective observational study enrolled 60 patients with LHON between January 2015 and December 2021. The abnormal MRI features seen in the pregeniculate visual pathway were investigated, and then correlated with the causative mitochondrial DNA (mtDNA) mutation, the distribution of the MRI lesions and the duration of vision loss. Result: The cohort included 48 (80%) males and 53 (88%) had bilateral vision loss. The median age of onset was 17.0 years (range 4.0-58.0). 28 (47%) patients had the m.11778G>A mutation. 34 (57%) patients had T2 hyperintensity (HS) in the pregeniculate visual pathway and 13 (22%) patients with chiasmal enlargement. 20 patients (71%) carrying the m.11778G>A mutation had T2 HS, significantly more than the 14 patients (44%) with T2 HS in the other LHON mutation groups (p=0.039). Furthermore, significantly more patients in the m.11778G>A group (16 patients (57%)) had T2 HS in optic chiasm (OCh)/optic tract (OTr) than the other LHON mutation groups (7 patients (22%), p=0.005). Optic chiasmal enlargement was more common in patients with vision loss duration <3 months compared with those ≥3 months (p=0.028). Conclusion: T2 HS in the pregeniculate visual pathway is a frequent finding in LHON. Signal changes in the OCh/OTr and chiasmal enlargement, in particular within the first 3 months of visual loss, were more commonly seen in patients carrying the m.11778G>A mtDNA mutation, which may be of diagnostic significance.
Language	English
Publishing date	2024-01-17
Publishing country	England
Document type	Journal Article
ZDB-ID	80078-8
ISSN	1468-2079 ; 0007-1161
ISSN (online)	1468-2079
ISSN	0007-1161
DOI	10.1136/bjo-2023-324628
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Article ; Online: The diagnostic accuracy of photopic negative responses evoked by broadband and chromatic stimuli in a clinically heterogeneous population.

Leo, Shaun M / Neveu, Magella M / Yu-Wai-Man, Patrick / Mahroo, Omar A / Robson, Anthony G

Documenta ophthalmologica. Advances in ophthalmology

2023 Volume 147, Issue 3, Page(s) 165–177

Abstract: ... a statistically significant difference between sensitivities (p = 0.046) but not specificities (p = 0.08 ...

Abstract	Purpose: To compare the diagnostic accuracy of the photopic negative response (PhNR) elicited by red-blue (RB) and white-white (WW) stimuli, for detection of retinal ganglion cell (RGC) dysfunction in a heterogeneous clinical cohort. Methods: Adults referred for electrophysiological investigations were recruited consecutively for this single-centre, prospective, paired diagnostic accuracy study. PhNRs were recorded to red flashes (1.5 cd·s·m Results: Two hundred and forty-three participants were initially enrolled, with 200 (median age 54; range 18-95; female 65%) meeting inclusion criteria. Sensitivity was 53% (95% confidence intervals [CI] 39% to 68%) and 62% (95% CI 48% to 76%), for WW and RB PhNRs, respectively. Specificity was 80% (95% CI 74% to 86%) and 78% (95% CI 72% to 85%), respectively. There was a statistically significant difference between sensitivities (p = 0.046) but not specificities (p = 0.08) of the two methods. Receiver operator characteristic (ROC) area under the curve (AUC) values were 0.73 for WW and 0.74 for RB PhNRs. Conclusion: PhNRs to red flashes on a blue background may be more sensitive than white-on-white stimuli, but there is no significant difference between specificities. This study highlights the value and potential convenience of using white-on-white stimuli, already used widely for routine ERG assessment.
MeSH term(s)	Adult ; Humans ; Female ; Middle Aged ; Electroretinography/methods ; Prospective Studies ; Evoked Potentials, Visual ; Retina/physiology ; Retinal Ganglion Cells/physiology ; Photic Stimulation
Language	English
Publishing date	2023-10-27
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	212594-8
ISSN	1573-2622 ; 0012-4486
ISSN (online)	1573-2622
ISSN	0012-4486
DOI	10.1007/s10633-023-09956-5
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Article ; Online: Characterisation of a novel OPA1 splice variant resulting in cryptic splice site activation and mitochondrial dysfunction.

Harvey, Joshua Paul / Yu-Wai-Man, Patrick / Cheetham, Michael Edward

European journal of human genetics : EJHG

2022 Volume 30, Issue 7, Page(s) 848–855

Abstract: ... specifically a 21 base pair deletion at the start of exon 24, NM_015560.2(OPA1):p.Cys786_Lys792del ...

Abstract	Autosomal dominant optic atrophy (DOA) is an inherited optic neuropathy that results in progressive, bilateral visual acuity loss and field defects. OPA1 is the causative gene in around 60% of cases of DOA. The majority of patients have a pure ocular phenotype, but 20% have extra-ocular features (DOA +). We report on a patient with DOA + manifesting as bilateral optic atrophy, spastic paraparesis, urinary incontinence and white matter changes in the central nervous system associated with a novel heterozygous splice variant NM_015560.2(OPA1):c.2356-1 G > T. Further characterisation, which was performed using fibroblasts obtained from a skin biopsy, demonstrated that this variant altered mRNA splicing of the OPA1 transcript, specifically a 21 base pair deletion at the start of exon 24, NM_015560.2(OPA1):p.Cys786_Lys792del. The majority of variant transcripts were shown to escape nonsense-mediated decay and modelling of the predicted protein structure suggests that the in-frame 7 amino acid deletion may affect OPA1 oligomerisation. Fibroblasts carrying the c.2356-1 G > T variant demonstrated impaired mitochondrial bioenergetics, membrane potential, increased cell death, and disrupted and fragmented mitochondrial networks in comparison to WT cells. This study suggests that the c.2356-1 G > T OPA1 splice site variant leads to a cryptic splice site activation and may manifest in a dominant-negative manner, which could account for the patient's severe syndromic phenotype.
MeSH term(s)	GTP Phosphohydrolases/genetics ; Humans ; Mitochondria/genetics ; Mitochondria/pathology ; Mutation ; Optic Atrophy, Autosomal Dominant/genetics ; Optic Atrophy, Autosomal Dominant/pathology ; RNA Splice Sites
Chemical Substances	RNA Splice Sites ; GTP Phosphohydrolases (EC 3.6.1.-) ; OPA1 protein, human (EC 3.6.1.-)
Language	English
Publishing date	2022-05-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1141470-4
ISSN	1476-5438 ; 1018-4813
ISSN (online)	1476-5438
ISSN	1018-4813
DOI	10.1038/s41431-022-01102-0
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Article ; Online: Developments in the Treatment of Leber Hereditary Optic Neuropathy.

Chen, Benson S / Yu-Wai-Man, Patrick / Newman, Nancy J

Current neurology and neuroscience reports

2022 Volume 22, Issue 12, Page(s) 881–892

Abstract: Purposeof review: To outline the current landscape of treatments for Leber hereditary optic neuropathy (LHON) along the therapeutic delivery pipeline, exploring the mechanisms of action and evidence for these therapeutic approaches.: Recent findings: ...

Abstract	Purposeof review: To outline the current landscape of treatments for Leber hereditary optic neuropathy (LHON) along the therapeutic delivery pipeline, exploring the mechanisms of action and evidence for these therapeutic approaches. Recent findings: Treatments for LHON can be broadly classified as either mutation-specific or mutation-independent. Mutation-specific therapies aim to correct the underlying mutation through the use of a gene-editing platform or replace the faulty mitochondrial DNA-encoded protein by delivering the wild-type gene using a suitable vector. Recent gene therapy clinical trials assessing the efficacy of allotopically expressed MT-ND4 for the treatment of LHON due to the m.11778G > A mutation in MT-ND4 have shown positive results when treated within 12 months of symptom onset. Mutation-independent therapies can have various downstream targets that aim to improve mitochondrial respiration, reduce mitochondrial stress, inhibit or delay retinal ganglion cell apoptosis, and/or promote retinal ganglion cell survival. Idebenone, a synthetic hydrosoluble analogue of co-enzyme Q
MeSH term(s)	Humans ; Optic Atrophy, Hereditary, Leber/genetics ; Optic Atrophy, Hereditary, Leber/therapy ; Optic Atrophy, Hereditary, Leber/diagnosis ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/metabolism ; DNA, Mitochondrial/therapeutic use ; Retinal Ganglion Cells ; Mitochondria/genetics ; Mutation
Chemical Substances	DNA, Mitochondrial
Language	English
Publishing date	2022-11-21
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2057363-7
ISSN	1534-6293 ; 1528-4042
ISSN (online)	1534-6293
ISSN	1528-4042
DOI	10.1007/s11910-022-01246-y
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