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| Optic neuropathy v6.14 | NDUFAF8 | Ida Ertmanska changed review comment from: Comment on list classification: There are at least 6 individuals from 3 unrelated individuals reported in literature with biallelic NDUFAF8 variants and optic atrophy - isolated or syndromic. Hence, this gene should be promoted to Green at the next GMS update.; to: Comment on list classification: There are at least 6 individuals from 3 unrelated families reported in literature with biallelic NDUFAF8 variants and optic atrophy - isolated or syndromic. Hence, this gene should be promoted to Green at the next GMS update. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Optic neuropathy v6.14 | NDUFAF8 |
Ida Ertmanska changed review comment from: PMID: 41234160 Fiorini et al., 2025 Authors identified candidate causative variants in 31 patients from 23 unrelated families, with biallelic or hemizygous variants in 11 different nuclear Complex I related genes. 5/6 patients reported with NDUFAF8 variants had isolated optic atrophy; the sixth proband had OA plus nystagmus and cerebellar ataxia. Family U - 2 sibs hom for c.44T>G p.(L15R) - isolated OA, MRI normal Families W & V (4 individuals from 2 families)- hom for c.195+271C>T p.? deep intronic variant - insidious isolated OA in family W, individuals in Family V had LHON-like presentation of OA + strabismus, hyperopia, non-specific white matter lesions on MRI (3/3), also mild DD, nystagmus, and unsteady gate in 1/3. This gene is associated with AR Mitochondrial complex I deficiency, nuclear type 34, OMIM:618776 (accessed 26th May 2026).; to: PMID: 41234160 Fiorini et al., 2025 Authors identified candidate causative variants in 31 patients from 23 unrelated families, with biallelic or hemizygous variants in 11 different nuclear Complex I related genes. 5/6 patients reported with NDUFAF8 variants had isolated optic atrophy; the sixth proband had OA plus nystagmus and cerebellar ataxia. Family U - 2 sibs hom for c.44T>G p.(L15R) - isolated OA, MRI normal Families W & V (4 individuals from 2 families)- hom for c.195+271C>T p.? deep intronic variant - insidious isolated OA in family W, individuals in Family V had LHON-like presentation of OA + strabismus, hyperopia, non-specific white matter lesions on MRI (3/3), also mild DD, nystagmus, and unsteady gate in 1/3. This gene is associated with AR Mitochondrial complex I deficiency, nuclear type 34, OMIM:618776 (accessed 26th May 2026). |
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| Optic neuropathy v6.14 | NDUFAF8 | Achchuthan Shanmugasundram Tag Q2_26_NHS_review tag was added to gene: NDUFAF8. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Optic neuropathy v6.14 | NDUFAF8 | Ida Ertmanska Phenotypes for gene: NDUFAF8 were changed from Optic neuropathy, optic atrophy; LHON-like to Mitochondrial complex I deficiency, nuclear type 34, OMIM:618776 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Optic neuropathy v6.13 | NDUFAF8 | Ida Ertmanska Publications for gene: NDUFAF8 were set to PMID: 41234160 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Optic neuropathy v6.12 | NDUFAF8 | Ida Ertmanska Classified gene: NDUFAF8 as Amber List (moderate evidence) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Optic neuropathy v6.12 | NDUFAF8 | Ida Ertmanska Added comment: Comment on list classification: There are at least 6 individuals from 3 unrelated individuals reported in literature with biallelic NDUFAF8 variants and optic atrophy - isolated or syndromic. Hence, this gene should be promoted to Green at the next GMS update. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Optic neuropathy v6.12 | NDUFAF8 | Ida Ertmanska Gene: ndufaf8 has been classified as Amber List (Moderate Evidence). | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Optic neuropathy v6.11 | NDUFAF8 | Ida Ertmanska Tag Q2_26_promote_green tag was added to gene: NDUFAF8. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Optic neuropathy v6.11 | NDUFAF8 | Ida Ertmanska reviewed gene: NDUFAF8: Rating: GREEN; Mode of pathogenicity: None; Publications: 41234160; Phenotypes: Mitochondrial complex I deficiency, nuclear type 34, OMIM:618776; Mode of inheritance: BIALLELIC, autosomal or pseudoautosomal | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Optic neuropathy v5.26 | NDUFAF8 |
Neringa Jurkute gene: NDUFAF8 was added gene: NDUFAF8 was added to Optic neuropathy. Sources: Literature,Research Mode of inheritance for gene: NDUFAF8 was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: NDUFAF8 were set to PMID: 41234160 Phenotypes for gene: NDUFAF8 were set to Optic neuropathy, optic atrophy; LHON-like Mode of pathogenicity for gene: NDUFAF8 was set to Other Review for gene: NDUFAF8 was set to GREEN Added comment: Recently accepted publication "Recessive variants in mitochondrial Complex I nuclear subunits are an underrated cause of optic atrophy" reports Complex I genes, which pathogenic defects lead to optic atrophy; LHON-like phenotypes. 3 unrelated families were carrying NDUFS7 pathogenic variants and were diagnoses with optic neuropathy Defects in core CI subunits in reported cohort lead to isolated optic atrophy, while defects in accessory CI subunits and assembly factors resulted in a spectrum of phenotypes, from isolated to syndromic optic atrophy. For 12 cases, the subacute onset of vision loss enabled us to associate or confirm novel genes (NDUFS7, NDUFV1, NDUFAF2, NDUFAF4, NDUFAF8) with the autosomal recessive Leber Hereditary Optic Neuropathy (arLHON) phenotype. Moreover, in the NDUFS7 subunit a partial spatial segregation was noted for missense variants causing either Leigh syndrome or isolated optic atrophy, hinting at possible disease-specific molecular defect. Sources: Literature, Research |
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| Optic neuropathy v5.26 | NDUFAF4 |
Neringa Jurkute gene: NDUFAF4 was added gene: NDUFAF4 was added to Optic neuropathy. Sources: Literature,Research Mode of inheritance for gene: NDUFAF4 was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: NDUFAF4 were set to PMID: 41234160 Phenotypes for gene: NDUFAF4 were set to Optic neuropathy, optic atrophy; LHON-like Mode of pathogenicity for gene: NDUFAF4 was set to Other Review for gene: NDUFAF4 was set to GREEN Added comment: Recently accepted publication "Recessive variants in mitochondrial Complex I nuclear subunits are an underrated cause of optic atrophy" reports Complex I genes, which pathogenic defects lead to optic atrophy; LHON-like phenotypes. 2 unrelated families were carrying NDUFS7 pathogenic variants and were diagnoses with optic neuropathy Defects in core CI subunits in reported cohort lead to isolated optic atrophy, while defects in accessory CI subunits and assembly factors resulted in a spectrum of phenotypes, from isolated to syndromic optic atrophy. For 12 cases, the subacute onset of vision loss enabled us to associate or confirm novel genes (NDUFS7, NDUFV1, NDUFAF2, NDUFAF4, NDUFAF8) with the autosomal recessive Leber Hereditary Optic Neuropathy (arLHON) phenotype. Moreover, in the NDUFS7 subunit a partial spatial segregation was noted for missense variants causing either Leigh syndrome or isolated optic atrophy, hinting at possible disease-specific molecular defect. Sources: Literature, Research |
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| Optic neuropathy v5.26 | NDUFAF3 |
Neringa Jurkute gene: NDUFAF3 was added gene: NDUFAF3 was added to Optic neuropathy. Sources: Literature,Research Mode of inheritance for gene: NDUFAF3 was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: NDUFAF3 were set to PMID: 41234160 Phenotypes for gene: NDUFAF3 were set to Optic neuropathy, optic atrophy; LHON-like Mode of pathogenicity for gene: NDUFAF3 was set to Other Review for gene: NDUFAF3 was set to GREEN Added comment: Recently accepted publication "Recessive variants in mitochondrial Complex I nuclear subunits are an underrated cause of optic atrophy" reports Complex I genes, which pathogenic defects lead to optic atrophy; LHON-like phenotypes. 1 family were carrying NDUFAF3 pathogenic variants and affected individual was diagnoses with optic neuropathy Defects in core CI subunits in reported cohort lead to isolated optic atrophy, while defects in accessory CI subunits and assembly factors resulted in a spectrum of phenotypes, from isolated to syndromic optic atrophy. For 12 cases, the subacute onset of vision loss enabled us to associate or confirm novel genes (NDUFS7, NDUFV1, NDUFAF2, NDUFAF4, NDUFAF8) with the autosomal recessive Leber Hereditary Optic Neuropathy (arLHON) phenotype. Moreover, in the NDUFS7 subunit a partial spatial segregation was noted for missense variants causing either Leigh syndrome or isolated optic atrophy, hinting at possible disease-specific molecular defect. Sources: Literature, Research |
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| Optic neuropathy v5.26 | NDUFAF2 |
Neringa Jurkute gene: NDUFAF2 was added gene: NDUFAF2 was added to Optic neuropathy. Sources: Literature,Research Mode of inheritance for gene: NDUFAF2 was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: NDUFAF2 were set to PMID: 41234160 Phenotypes for gene: NDUFAF2 were set to Optic neuropathy, optic atrophy; LHON-like Mode of pathogenicity for gene: NDUFAF2 was set to Other Review for gene: NDUFAF2 was set to GREEN Added comment: Recently accepted publication "Recessive variants in mitochondrial Complex I nuclear subunits are an underrated cause of optic atrophy" reports Complex I genes, which pathogenic defects lead to optic atrophy; LHON-like phenotypes. 2 unrelated families were carrying NDUFAF2 pathogenic variants and were diagnoses with optic neuropathy Defects in core CI subunits in reported cohort lead to isolated optic atrophy, while defects in accessory CI subunits and assembly factors resulted in a spectrum of phenotypes, from isolated to syndromic optic atrophy. For 12 cases, the subacute onset of vision loss enabled us to associate or confirm novel genes (NDUFS7, NDUFV1, NDUFAF2, NDUFAF4, NDUFAF8) with the autosomal recessive Leber Hereditary Optic Neuropathy (arLHON) phenotype. Moreover, in the NDUFS7 subunit a partial spatial segregation was noted for missense variants causing either Leigh syndrome or isolated optic atrophy, hinting at possible disease-specific molecular defect. Sources: Literature, Research |
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| Optic neuropathy v5.26 | NDUFB11 |
Neringa Jurkute gene: NDUFB11 was added gene: NDUFB11 was added to Optic neuropathy. Sources: Literature,Research Mode of inheritance for gene: NDUFB11 was set to X-LINKED: hemizygous mutation in males, biallelic mutations in females Publications for gene: NDUFB11 were set to PMID: 41234160 Phenotypes for gene: NDUFB11 were set to Optic neuropathy, optic atrophy; LHON-like Mode of pathogenicity for gene: NDUFB11 was set to Other Review for gene: NDUFB11 was set to GREEN Added comment: Recently accepted publication "Recessive variants in mitochondrial Complex I nuclear subunits are an underrated cause of optic atrophy" reports Complex I genes, which pathogenic defects lead to optic atrophy; LHON-like phenotypes. 1 family were carrying NDUFB11 pathogenic variant and affected individual was diagnoses with optic neuropathy Defects in core CI subunits in reported cohort lead to isolated optic atrophy, while defects in accessory CI subunits and assembly factors resulted in a spectrum of phenotypes, from isolated to syndromic optic atrophy. For 12 cases, the subacute onset of vision loss enabled us to associate or confirm novel genes (NDUFS7, NDUFV1, NDUFAF2, NDUFAF4, NDUFAF8) with the autosomal recessive Leber Hereditary Optic Neuropathy (arLHON) phenotype. Moreover, in the NDUFS7 subunit a partial spatial segregation was noted for missense variants causing either Leigh syndrome or isolated optic atrophy, hinting at possible disease-specific molecular defect. Sources: Literature, Research |
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| Optic neuropathy v5.26 | NDUFA10 |
Neringa Jurkute gene: NDUFA10 was added gene: NDUFA10 was added to Optic neuropathy. Sources: Literature,Research Mode of inheritance for gene: NDUFA10 was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: NDUFA10 were set to PMID: 41234160 Phenotypes for gene: NDUFA10 were set to Optic neuropathy, optic atrophy; LHON-like Mode of pathogenicity for gene: NDUFA10 was set to Other Review for gene: NDUFA10 was set to GREEN Added comment: Recently accepted publication "Recessive variants in mitochondrial Complex I nuclear subunits are an underrated cause of optic atrophy" reports Complex I genes, which pathogenic defects lead to optic atrophy; LHON-like phenotypes. 3 unrelated families were carrying NDUFA10 pathogenic variants and were diagnoses with optic neuropathy Defects in core CI subunits in reported cohort lead to isolated optic atrophy, while defects in accessory CI subunits and assembly factors resulted in a spectrum of phenotypes, from isolated to syndromic optic atrophy. For 12 cases, the subacute onset of vision loss enabled us to associate or confirm novel genes (NDUFS7, NDUFV1, NDUFAF2, NDUFAF4, NDUFAF8) with the autosomal recessive Leber Hereditary Optic Neuropathy (arLHON) phenotype. Moreover, in the NDUFS7 subunit a partial spatial segregation was noted for missense variants causing either Leigh syndrome or isolated optic atrophy, hinting at possible disease-specific molecular defect. Sources: Literature, Research |
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| Optic neuropathy v5.26 | NDUFA1 |
Neringa Jurkute gene: NDUFA1 was added gene: NDUFA1 was added to Optic neuropathy. Sources: Literature,Research Mode of inheritance for gene: NDUFA1 was set to X-LINKED: hemizygous mutation in males, biallelic mutations in females Publications for gene: NDUFA1 were set to PMID: 41234160 Phenotypes for gene: NDUFA1 were set to Optic neuropathy, optic atrophy; LHON-like Mode of pathogenicity for gene: NDUFA1 was set to Other Review for gene: NDUFA1 was set to GREEN Added comment: Recently accepted publication "Recessive variants in mitochondrial Complex I nuclear subunits are an underrated cause of optic atrophy" reports Complex I genes, which pathogenic defects lead to optic atrophy; LHON-like phenotypes. 3 unrelated families were carrying NDUFA1 pathogenic variants and were diagnoses with optic neuropathy Defects in core CI subunits in reported cohort lead to isolated optic atrophy, while defects in accessory CI subunits and assembly factors resulted in a spectrum of phenotypes, from isolated to syndromic optic atrophy. For 12 cases, the subacute onset of vision loss enabled us to associate or confirm novel genes (NDUFS7, NDUFV1, NDUFAF2, NDUFAF4, NDUFAF8) with the autosomal recessive Leber Hereditary Optic Neuropathy (arLHON) phenotype. Moreover, in the NDUFS7 subunit a partial spatial segregation was noted for missense variants causing either Leigh syndrome or isolated optic atrophy, hinting at possible disease-specific molecular defect. Sources: Literature, Research |
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| Optic neuropathy v5.26 | NDUFV2 |
Neringa Jurkute gene: NDUFV2 was added gene: NDUFV2 was added to Optic neuropathy. Sources: Literature,Research Mode of inheritance for gene: NDUFV2 was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: NDUFV2 were set to PMID: 41234160 Phenotypes for gene: NDUFV2 were set to Optic neuropathy, optic atrophy; LHON-like Mode of pathogenicity for gene: NDUFV2 was set to Other Review for gene: NDUFV2 was set to GREEN Added comment: Recently accepted publication "Recessive variants in mitochondrial Complex I nuclear subunits are an underrated cause of optic atrophy" reports Complex I genes, which pathogenic defects lead to optic atrophy; LHON-like phenotypes. 1 family was carrying NDUFV2 pathogenic variant and affected individual was diagnoses with optic neuropathy Defects in core CI subunits in reported cohort lead to isolated optic atrophy, while defects in accessory CI subunits and assembly factors resulted in a spectrum of phenotypes, from isolated to syndromic optic atrophy. For 12 cases, the subacute onset of vision loss enabled us to associate or confirm novel genes (NDUFS7, NDUFV1, NDUFAF2, NDUFAF4, NDUFAF8) with the autosomal recessive Leber Hereditary Optic Neuropathy (arLHON) phenotype. Moreover, in the NDUFS7 subunit a partial spatial segregation was noted for missense variants causing either Leigh syndrome or isolated optic atrophy, hinting at possible disease-specific molecular defect. Sources: Literature, Research |
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| Optic neuropathy v5.26 | NDUFV1 |
Neringa Jurkute gene: NDUFV1 was added gene: NDUFV1 was added to Optic neuropathy. Sources: Literature,Research Mode of inheritance for gene: NDUFV1 was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: NDUFV1 were set to PMID: 41234160 Phenotypes for gene: NDUFV1 were set to Optic neuropathy, optic atrophy; LHON-like Mode of pathogenicity for gene: NDUFV1 was set to Other Review for gene: NDUFV1 was set to GREEN Added comment: Recently accepted publication "Recessive variants in mitochondrial Complex I nuclear subunits are an underrated cause of optic atrophy" reports Complex I genes, which pathogenic defects lead to optic atrophy; LHON-like phenotypes. 1 family was carrying NDUFV1 pathogenic variant and affected individual was diagnoses with optic neuropathy Defects in core CI subunits in reported cohort lead to isolated optic atrophy, while defects in accessory CI subunits and assembly factors resulted in a spectrum of phenotypes, from isolated to syndromic optic atrophy. For 12 cases, the subacute onset of vision loss enabled us to associate or confirm novel genes (NDUFS7, NDUFV1, NDUFAF2, NDUFAF4, NDUFAF8) with the autosomal recessive Leber Hereditary Optic Neuropathy (arLHON) phenotype. Moreover, in the NDUFS7 subunit a partial spatial segregation was noted for missense variants causing either Leigh syndrome or isolated optic atrophy, hinting at possible disease-specific molecular defect. Sources: Literature, Research |
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| Optic neuropathy v5.26 | NDUFS7 |
Neringa Jurkute gene: NDUFS7 was added gene: NDUFS7 was added to Optic neuropathy. Sources: Literature,Research Mode of inheritance for gene: NDUFS7 was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: NDUFS7 were set to PMID: 41234160 Phenotypes for gene: NDUFS7 were set to Optic neuropathy; optic atrophy; LHON-like Mode of pathogenicity for gene: NDUFS7 was set to Other Review for gene: NDUFS7 was set to GREEN Added comment: Recently accepted publication "Recessive variants in mitochondrial Complex I nuclear subunits are an underrated cause of optic atrophy" reports Complex I genes, which pathogenic defects lead to optic atrophy; LHON-like phenotypes. 5 unrelated families were carrying NDUFS7 pathogenic variants and were diagnoses with optic neuropathy Defects in core CI subunits in reported cohort lead to isolated optic atrophy, while defects in accessory CI subunits and assembly factors resulted in a spectrum of phenotypes, from isolated to syndromic optic atrophy. For 12 cases, the subacute onset of vision loss enabled us to associate or confirm novel genes (NDUFS7, NDUFV1, NDUFAF2, NDUFAF4, NDUFAF8) with the autosomal recessive Leber Hereditary Optic Neuropathy (arLHON) phenotype. Moreover, in the NDUFS7 subunit a partial spatial segregation was noted for missense variants causing either Leigh syndrome or isolated optic atrophy, hinting at possible disease-specific molecular defect. Sources: Literature, Research |
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