Evidence map›Paper›PMID 27150940›Full record

ReviewMolecular medicine reports2016

Recessive optic atrophy, sensorimotor neuropathy and cataract associated with novel compound heterozygous mutations in OPA1.

Jinho Lee, Sung-Chul Jung, Young Bin Hong, Jeong Hyun Yoo, Heasoo Koo, Ja Hyun Lee, Hyun Dae Hong, Sang-Beom Kim, Ki Wha Chung, Byung-Ok Choi

Open access · hybridAbstract readCase ReportsReview
In one paragraph

Review in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 20% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Compound Heterozygous Mutations ofInternational journal of molecular sciences · 2024
    Article
  3. Article
  4. Review
  5. Mitochondrial Retinopathies.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 1 country.

Jinho LeeDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 135‑710, Republic of Korea.
Sung-Chul JungDepartment of Biochemistry, Ewha Womans University School of Medicine, Seoul 120‑750, Republic of Korea.
Young Bin HongDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 135‑710, Republic of Korea.
Jeong Hyun YooDepartment of Radiology, Ewha Womans University School of Medicine, Seoul 120‑750, Republic of Korea.
Heasoo KooDepartment of Pathology, Ewha Womans University School of Medicine, Seoul 120‑750, Republic of Korea.
Ja Hyun LeeDepartment of Biological Science, Kongju National University, Konju, Chungnam 314‑701, Republic of Korea.
Hyun Dae HongDepartment of Biological Science, Kongju National University, Konju, Chungnam 314‑701, Republic of Korea.
Sang-Beom KimDepartment of Neurology, Kyung Hee University College of Medicine, Seoul 143‑601, Republic of Korea.
Ki Wha ChungDepartment of Biological Science, Kongju National University, Konju, Chungnam 314‑701, Republic of Korea.
Byung-Ok ChoiDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 135‑710, Republic of Korea.
Ewha Womans University · KRKongju National University · KRSamsung Medical Center · KRKyung Hee University · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the optic atrophy 1 gene (OPA1) are associated with autosomal dominant optic atrophy and 20% of patients demonstrate extra-ocular manifestations. In addition to these autosomal dominant cases, only a few syndromic cases have been reported thus far with compound heterozygous OPA1 mutations, suggestive of either recessive or semi‑dominant patterns of inheritance. The majority of these patients were diagnosed with Behr syndrome, characterized by optic atrophy, ataxia and peripheral neuropathy. The present study describes a 10-year-old boy with Behr syndrome presenting with early‑onset severe optic atrophy, sensorimotor neuropathy, ataxia and congenital cataracts. He had optic atrophy and was declared legally blind at six years old. Electrophysiological, radiological, and histopathological findings were compatible with axonal sensorimotor polyneuropathy. At birth, he presented with a congenital cataract, which has not been previously described in patients with OPA1 mutations. Whole exome sequencing indicated a pair of novel compound heterozygous mutations: p.L620fs*13 (c.1857‑1858delinsT) and p.R905Q (c.G2714A). Neither mutation was observed in controls (n=300), and thus, they were predicted to be pathogenic by multiple in silico analyses. The mutation sites were highly conserved throughout different vertebrate species. The patients parents did not have any ophthalmic or neurologic symptoms and the results of electrophysiological studies were normal, suggestive of an autosomal recessive pattern of inheritance. The present study identified novel compound heterozygous OPA1 mutations in a patient with recessive optic atrophy, sensorimotor neuropathy and congenital cataracts, indicating an expansion of the clinical spectrum of pathologies associated with OPA1 mutations. Thus, OPA1 gene screening is advisable in the workup of patients with recessive optic atrophy, particularly with Behr syndrome and cataracts.

Indexed as

HeterozygoteMutationAtaxiaBiopsyCataractChildDNA Mutational AnalysisExomeGenes, RecessiveGTP PhosphohydrolasesHearing LossHigh-Throughput Nucleotide SequencingHumansIntellectual DisabilityLegMagnetic Resonance ImagingGTP PhosphohydrolasesOPA1 protein, human

Identifiers

PMID27150940
PMCPMC4918608
OpenAlexW2346606510

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

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.