Evidence map›Paper›PMID 40014158›Full record

ArticleNeurogenetics2025

The fourth family in the world with a novel variant in the ATP5MK gene: four siblings with complex V (ATP synthase) deficiency.

Rojan İpek, Akçahan Akalın, Esra Habiloğlu, Salih Hattapoğlu, Ayfer Gözü Pirinççioğlu

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Article in Neurogenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
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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

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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

2 citing papers in PubMed.

  1. Dystonia: Insights into Mechanisms and Novel Therapeutics.Current neurology and neuroscience reports · 2026
    Review
  2. Article
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

5 authors.

Rojan İpekDepartment of Pediatric Neurology, Dicle University, Diyarbakır, Türkiye. rjnipek@hotmail.com.
Akçahan AkalınDepartment of Pediatric Genetics, DiyarbakıR Childrens Diseases Hospital, Diyarbakır, Türkiye.
Esra HabiloğluDepartment of Medical Genetics, Batman Training and Research Hospital, Batman, Türkiye.
Salih HattapoğluDepartment of Radiology, Dicle University, Diyarbakır, Türkiye.
Ayfer Gözü PirinççioğluDepartment of Pediatric Health and Diseases, Dicle University, Diyarbakır, Türkiye.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial Complex V (ATP synthase) deficiency nuclear type 6 (MC5DN6) is a progressive neurodegenerative disorder characterized by autosomal recessive inheritance and developmental regression, particularly in gross motor skills, which manifests in early childhood. This study aims to present the discovery of a novel variant in four male siblings aged 13 years 9 months to 25 years, making this the fourth family reported globally, while also raising awareness of rare mitochondrial diseases. Four individuals from the same family were retrospectively evaluated based on their demographic, clinical, laboratory, and molecular genetic data. The mutation in the ATP5MK gene was analyzed using the exome sequencing (ES) method. The detected variation was classified according to the criteria American College of Medical Genetics. Four cases, aged between 13 years 9 months and 25 years, were analyzed. All individuals were male. While all four cases had a history of neurodegenerative disease, they also exhibited intellectual disability, muscle weakness, increased deep tendon reflexes in the lower extremities, spasticity, scoliosis, pes cavus deformity, positive Babinski reflex, abnormal gait patterns due to foot deformities, and normal cerebellar tests. Additional findings included geographic tongue (n = 2), strabismus (n = 2), nystagmus (n = 1), ophthalmoplegia (n = 2), hypertrophic upper extremity muscle body build (n = 2), keloid tissue (n = 1), and short stature (n = 3). ES of the first case identified a homozygous splice donor variant (c.87 + 1G > A) in the ATP5MK gene as a novel variant, and family screening revealed the same variant in a biallelic state in the other three siblings. The parents were confirmed as heterozygous carriers, consistent with autosomal recessive inheritance. Mitochondrial diseases can mimic a wide range of neurological disorders. They should be considered as a potential underlying cause when treatment for suspected differential diagnoses proves ineffective.

Indexed as

Mitochondrial DiseasesMitochondrial Proton-Translocating ATPasesAdolescentAdultExome SequencingHumansMaleMutationNeurodegenerative DiseasesPedigreeSiblingsYoung AdultMitochondrial Proton-Translocating ATPasesATP5MK geneMitochondrial complexNeurodegeneration

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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.