Evidence map›Paper›PMID 33909173›Full record

ReviewNeurogenetics2021

A novel pathogenic variant in the 3' end of the AGTPBP1 gene gives rise to neurodegeneration without cerebellar atrophy: an expansion of the disease phenotype?

Sevim Türay, Recep Eröz, A Nazlı Başak

Open access · greenAbstract readCase ReportsReview
PubMed Publisher
In one paragraph

Review in Neurogenetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. International journal of molecular sciences · 2022
    Article
  5. Review
  6. Autopsy Findings inCase reports in neurology
    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

3 authors at 2 institutions in 1 country.

Sevim TürayDepartment of Pediatric Neurology, Düzce University Medical Faculty, Duzce, 81820, Turkey. drsvm@yahoo.com.ORCID http://orcid.org/0000-0001-6002-052X
Recep ErözDepartment of Medical Genetics, Düzce University Medical Faculty, Duzce, Turkey.
A Nazlı BaşakSuna and İnan Kıraç Foundation, Neurodegeneration Research Laboratory, NDAL-KUTTAM, School of Medicine, Koç University, Istanbul, Turkey.
Düzce Üniversitesi · TRKoç University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Childhood-onset neurodegeneration with cerebellar atrophy (CONDCA) is a recently described form of the large group of infantile hereditary lower motor neuron diseases (Teoh et al. 2017), resulting from biallelic damaging variants in the AGTPBP1 gene, first described by Shashi et al. in EMBO J 37(23):e100540, 2018. AGTPBP-related neurodegeneration is a severe neurodevelopmental disorder that progresses with global developmental delay and intellectual disability, often accompanied with peripheral nerve damage and lower motor degeneration and a fatal course in the early years of life. The encoded protein is ATP/GTP-Binding Protein1, also known as cytosolic carboxypeptidase 1 (CCP1) or nervous system nuclear protein induced by axotomy (NNA1). Here we report a consanguineous family with four offspring, two of whom are affected. The index patient is a 21-month-old male with global developmental delay and hypotonia. The proband's 17-year-old sister, diagnosed with cerebral palsy, had severe hypotonia accompanied by motor and cognitive retardation. WES analysis revealed a novel homozygous c.3293G > A variant in the AGTPBP1 gene with high pathogenicity scores. Targeted Sanger sequencing confirmed the variant in both affected children and in heterozygous form in the parents. The affected siblings present with hypotonia and motor and cognitive retardation, in line with the studies previously reported. However, in our patients, no signs of cerebellar atrophy in cranial MRI were present, so the acronym CONDCA is not applicable; lower motor neuron findings were also absent. The matching and distinguishing aspects of our patients will add to the present literature and expand our understanding of this rare genetic neurodegenerative disease of early childhood.

Indexed as

Mutation, MissensePoint Mutation3' Untranslated RegionsAdolescentAnimalsCerebral PalsyConsanguinityDevelopmental DisabilitiesFemaleGTP-Binding ProteinsHomozygoteHumansInfantMagnetic Resonance ImagingMaleMuscle Hypotonia3' Untranslated RegionsAGTPBP1 protein, humanGTP-Binding ProteinsSerine-Type D-Ala-D-Ala CarboxypeptidaseAGTPBP1 geneAGTPBP1-related neurodegenerationHypotoniaMotor and cognitive retardation

Identifiers

PMID33909173
OpenAlexW3157946024

What OpenQuestion holds

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Registered trials

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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.