Evidence map›Paper›PMID 40788509›Full record

ArticleNeurogenetics2025

Whole exome sequencing identifies a novel variant causing Neurodegeneration with Brain Iron Accumulation syndrome (NBIA) in a consanguineous Pashtun family.

Hayat Khan, Muhammad Ilyas, Hina Qasim, Humaira Zeb, Muhammad Israr, Amjad Iqbal, Ahmad Ullah, Atta Ullah, Natalia Dominik, Henry Houlden and 2 more

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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
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

12 authors.

Hayat KhanCentre for Omic Sciences, Islamia College University Peshawar, Peshawar, Pakistan.
Muhammad IlyasCentre for Omic Sciences, Islamia College University Peshawar, Peshawar, Pakistan.
Hina QasimCentre for Omic Sciences, Islamia College University Peshawar, Peshawar, Pakistan.
Humaira ZebCentre for Omic Sciences, Islamia College University Peshawar, Peshawar, Pakistan.
Muhammad IsrarDepartment of Forensics, University of Swat, Swat, Pakistan.
Amjad IqbalDepartment of Medicine, Saidu Group of Teaching Hospitals, Swat, Swat, Pakistan.
Ahmad UllahCentre for Human Genetics, Hazara University Mansehra, Mansehra, Pakistan.
Atta UllahCentre for Human Genetics, Hazara University Mansehra, Mansehra, Pakistan.
Natalia DominikDepartment of Neuromuscular Disorders, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Henry HouldenDepartment of Neuromuscular Disorders, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK. h.houlden@ucl.ac.uk.
Stephanie EfthymiouDepartment of Neuromuscular Disorders, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Muhammad TariqNational Institute for Biotechnology and Genetic Engineering College, Pakistan Institute of Engineering and Applied Sciences (NIBGE-C, PIEAS), Faisalabad, Pakistan. tariqpalai@gmail.com.

Funding

Higher Education Commision, Pakistan NRPU-17341SYNaPS Study Group collaboration funded by The Wellcome Trust and strategic award WT093205 MA and WT104033AIA
6 · The paper itself

Abstract

Neurodegenerative disorders pose a significant public health problem. Among these, neurodegeneration with brain iron accumulation syndrome (NBIA) is particularly challenging because even MRI imaging findings can be subtle. Understanding the genetic basis of NBIA is, therefore, crucial for early diagnosis. This study aims to identify pathogenic mutations underlying NBIA in a consanguineous Pashtun family from Pakistan, using Next Generation Sequencing and protein structure modeling. Whole exome sequencing identified a novel pathogenic variant segregating in the family. Bioinformatics tools were employed for assessing the pathogenicity of the variant and 3D structure modelling of the protein. Following the filtration of variants according to the pedigree structure, we identified a novel homozygous variant (NM_001286611.1:c.1460A > C, p.Lys487Thr) in the REPS1 gene in the proband. Subsequent analysis confirmed the segregation of this variant within the family. Identification of this mutation expands our understanding of NBIA genetics and aids in early diagnosis. Stabilizing energy calculations support the impact of this variant on normal portion functioning.

Indexed as

Iron Metabolism DisordersNeurodegenerative DiseasesAdultBrainConsanguinityExome SequencingFemaleHumansMaleMutationNeuroaxonal DystrophiesPakistanPedigreeNBIANeurodegenerationREPS1Whole exome sequencing

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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.