Genotype-phenotype heterogeneity of ganglion cell and inner plexiform layer deficit in autosomal-dominant optic atrophy

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Genotype-phenotype heterogeneity of ganglion cell and inner plexiform layer deficit in autosomal-dominant optic atrophy. / Rönnbäck, Cecilia; Nissen, Claus; Almind, Gitte J; Grønskov, Karen; Milea, Dan; Larsen, Michael.

I: Acta Ophthalmologica, Bind 93, Nr. 8, 12.2015, s. 762-6.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Rönnbäck, C, Nissen, C, Almind, GJ, Grønskov, K, Milea, D & Larsen, M 2015, 'Genotype-phenotype heterogeneity of ganglion cell and inner plexiform layer deficit in autosomal-dominant optic atrophy', Acta Ophthalmologica, bind 93, nr. 8, s. 762-6. https://doi.org/10.1111/aos.12835

APA

Rönnbäck, C., Nissen, C., Almind, G. J., Grønskov, K., Milea, D., & Larsen, M. (2015). Genotype-phenotype heterogeneity of ganglion cell and inner plexiform layer deficit in autosomal-dominant optic atrophy. Acta Ophthalmologica, 93(8), 762-6. https://doi.org/10.1111/aos.12835

Vancouver

Rönnbäck C, Nissen C, Almind GJ, Grønskov K, Milea D, Larsen M. Genotype-phenotype heterogeneity of ganglion cell and inner plexiform layer deficit in autosomal-dominant optic atrophy. Acta Ophthalmologica. 2015 dec.;93(8):762-6. https://doi.org/10.1111/aos.12835

Author

Rönnbäck, Cecilia ; Nissen, Claus ; Almind, Gitte J ; Grønskov, Karen ; Milea, Dan ; Larsen, Michael. / Genotype-phenotype heterogeneity of ganglion cell and inner plexiform layer deficit in autosomal-dominant optic atrophy. I: Acta Ophthalmologica. 2015 ; Bind 93, Nr. 8. s. 762-6.

Bibtex

@article{bca43564c6fc400f9d3eeafbecac131f,
title = "Genotype-phenotype heterogeneity of ganglion cell and inner plexiform layer deficit in autosomal-dominant optic atrophy",
abstract = "PURPOSE: To describe the thickness of the combined ganglion cell and inner plexiform layers (GC-IPL) and the peripapillary retinal nerve fibre layer (RNFL) in patients with OPA1 c.983A>G or c.2708_2711delTTAG autosomal-dominant optic atrophy (ADOA).METHODS: The study included 20 individuals with c.983A>G and nine individuals with c.2708_2711delTTAG. Data for comparison were drawn from 49, previously published, individuals with OPA1 c.2826_2836delinsGGATGCTCCA and 51 individuals with no OPA1 mutation. Subjects underwent refraction, best-corrected visual acuity assessment, axial length measurement and high-definition optical coherence tomography.RESULTS: There was overlap in GC-IPL thickness in subjects younger than 20-30 years between the two new groups of ADOA patients and controls. Numerical decreases in GC-IPL thickness with age did not reach statistical significance in individuals with c.983A>G (p = 0.18) or in healthy controls (p = 0.22), but it did in individuals with c.2708_2711delTTAG (p = 0.02). Visual acuity decreased with decreasing GC-IPL thickness (p = 0.0006 in c.983A>G and p = 0.0084 in c.2708_2711delTTAG). Unlike c.2826_2836delinsGGATGCTCCA, individuals with c.983A>G or c.2708_2711delTTAG did not show a pattern of maximum GC-IPL deficit inferonasal of the fovea.CONCLUSION: Genotype-phenotype heterogeneity in OPA1 ADOA is evident when inner retinal atrophy is examined as a function of age. Thus, a pronounced decline with age in GC-IPL thickness is observed in c.2708_2711delTTAG ADOA, an intermediate decline with age is observed in c.983A>G ADOA, whereas little or no change with age is observed in c.2826_2836delinsGGATGCTCCA ADOA. This genotype-phenotype heterogeneity may explain why some patients have progressive visual loss while others have a relatively stable prognosis.",
author = "Cecilia R{\"o}nnb{\"a}ck and Claus Nissen and Almind, {Gitte J} and Karen Gr{\o}nskov and Dan Milea and Michael Larsen",
note = "{\textcopyright} 2015 Acta Ophthalmologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.",
year = "2015",
month = dec,
doi = "10.1111/aos.12835",
language = "English",
volume = "93",
pages = "762--6",
journal = "Acta Ophthalmologica",
issn = "1755-375X",
publisher = "Wiley-Blackwell",
number = "8",

}

RIS

TY - JOUR

T1 - Genotype-phenotype heterogeneity of ganglion cell and inner plexiform layer deficit in autosomal-dominant optic atrophy

AU - Rönnbäck, Cecilia

AU - Nissen, Claus

AU - Almind, Gitte J

AU - Grønskov, Karen

AU - Milea, Dan

AU - Larsen, Michael

N1 - © 2015 Acta Ophthalmologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.

PY - 2015/12

Y1 - 2015/12

N2 - PURPOSE: To describe the thickness of the combined ganglion cell and inner plexiform layers (GC-IPL) and the peripapillary retinal nerve fibre layer (RNFL) in patients with OPA1 c.983A>G or c.2708_2711delTTAG autosomal-dominant optic atrophy (ADOA).METHODS: The study included 20 individuals with c.983A>G and nine individuals with c.2708_2711delTTAG. Data for comparison were drawn from 49, previously published, individuals with OPA1 c.2826_2836delinsGGATGCTCCA and 51 individuals with no OPA1 mutation. Subjects underwent refraction, best-corrected visual acuity assessment, axial length measurement and high-definition optical coherence tomography.RESULTS: There was overlap in GC-IPL thickness in subjects younger than 20-30 years between the two new groups of ADOA patients and controls. Numerical decreases in GC-IPL thickness with age did not reach statistical significance in individuals with c.983A>G (p = 0.18) or in healthy controls (p = 0.22), but it did in individuals with c.2708_2711delTTAG (p = 0.02). Visual acuity decreased with decreasing GC-IPL thickness (p = 0.0006 in c.983A>G and p = 0.0084 in c.2708_2711delTTAG). Unlike c.2826_2836delinsGGATGCTCCA, individuals with c.983A>G or c.2708_2711delTTAG did not show a pattern of maximum GC-IPL deficit inferonasal of the fovea.CONCLUSION: Genotype-phenotype heterogeneity in OPA1 ADOA is evident when inner retinal atrophy is examined as a function of age. Thus, a pronounced decline with age in GC-IPL thickness is observed in c.2708_2711delTTAG ADOA, an intermediate decline with age is observed in c.983A>G ADOA, whereas little or no change with age is observed in c.2826_2836delinsGGATGCTCCA ADOA. This genotype-phenotype heterogeneity may explain why some patients have progressive visual loss while others have a relatively stable prognosis.

AB - PURPOSE: To describe the thickness of the combined ganglion cell and inner plexiform layers (GC-IPL) and the peripapillary retinal nerve fibre layer (RNFL) in patients with OPA1 c.983A>G or c.2708_2711delTTAG autosomal-dominant optic atrophy (ADOA).METHODS: The study included 20 individuals with c.983A>G and nine individuals with c.2708_2711delTTAG. Data for comparison were drawn from 49, previously published, individuals with OPA1 c.2826_2836delinsGGATGCTCCA and 51 individuals with no OPA1 mutation. Subjects underwent refraction, best-corrected visual acuity assessment, axial length measurement and high-definition optical coherence tomography.RESULTS: There was overlap in GC-IPL thickness in subjects younger than 20-30 years between the two new groups of ADOA patients and controls. Numerical decreases in GC-IPL thickness with age did not reach statistical significance in individuals with c.983A>G (p = 0.18) or in healthy controls (p = 0.22), but it did in individuals with c.2708_2711delTTAG (p = 0.02). Visual acuity decreased with decreasing GC-IPL thickness (p = 0.0006 in c.983A>G and p = 0.0084 in c.2708_2711delTTAG). Unlike c.2826_2836delinsGGATGCTCCA, individuals with c.983A>G or c.2708_2711delTTAG did not show a pattern of maximum GC-IPL deficit inferonasal of the fovea.CONCLUSION: Genotype-phenotype heterogeneity in OPA1 ADOA is evident when inner retinal atrophy is examined as a function of age. Thus, a pronounced decline with age in GC-IPL thickness is observed in c.2708_2711delTTAG ADOA, an intermediate decline with age is observed in c.983A>G ADOA, whereas little or no change with age is observed in c.2826_2836delinsGGATGCTCCA ADOA. This genotype-phenotype heterogeneity may explain why some patients have progressive visual loss while others have a relatively stable prognosis.

U2 - 10.1111/aos.12835

DO - 10.1111/aos.12835

M3 - Journal article

C2 - 26385429

VL - 93

SP - 762

EP - 766

JO - Acta Ophthalmologica

JF - Acta Ophthalmologica

SN - 1755-375X

IS - 8

ER -

ID: 161440633