Novel Homozygous Mutation of the AIMP1 Gene: A Milder Neuroimaging Phenotype With Preservation of the Deep White Matter.


Journal

Pediatric neurology
ISSN: 1873-5150
Titre abrégé: Pediatr Neurol
Pays: United States
ID NLM: 8508183

Informations de publication

Date de publication:
02 2019
Historique:
received: 25 07 2018
revised: 05 09 2018
accepted: 22 09 2018
pubmed: 28 11 2018
medline: 24 3 2020
entrez: 28 11 2018
Statut: ppublish

Résumé

Mutations in AIMP1, which plays an important role in the development and maintenance of axon-cytoskeleton integrity and regulating neurofilaments, cause neurodegeneration of variable severity and white matter abnormalities. From the patient records we analyzed the clinical evaluation, molecular genetics, neurodiagnostic, and neuroradiological investigations. We describe six members of a large consanguineous family with a phenotype of severe neurodegeneration in the form of developmental delays, progressive microcephaly, epilepsy, and failure to thrive. MRI showed callosal atrophy and T2 hyperintensity in the superficial white matter. The periventricular and deep white matter structures were, however, preserved. MR spectroscopy demonstrated N-acetylaspartate preservation without evidence of neuroinflammation. Exome sequencing showed a novel homozygous mutation of the AIMP1 gene in all individuals: c.917A>G (p.(Asp306Gly)). This novel homozygous mutation of the AIMP1 gene is characterized by preserved development of the periventricular and deep white matter structures as demonstrated by MRI and MR spectroscopy correlation.

Sections du résumé

BACKGROUND
Mutations in AIMP1, which plays an important role in the development and maintenance of axon-cytoskeleton integrity and regulating neurofilaments, cause neurodegeneration of variable severity and white matter abnormalities.
METHODS
From the patient records we analyzed the clinical evaluation, molecular genetics, neurodiagnostic, and neuroradiological investigations.
RESULTS
We describe six members of a large consanguineous family with a phenotype of severe neurodegeneration in the form of developmental delays, progressive microcephaly, epilepsy, and failure to thrive. MRI showed callosal atrophy and T2 hyperintensity in the superficial white matter. The periventricular and deep white matter structures were, however, preserved. MR spectroscopy demonstrated N-acetylaspartate preservation without evidence of neuroinflammation. Exome sequencing showed a novel homozygous mutation of the AIMP1 gene in all individuals: c.917A>G (p.(Asp306Gly)).
CONCLUSIONS
This novel homozygous mutation of the AIMP1 gene is characterized by preserved development of the periventricular and deep white matter structures as demonstrated by MRI and MR spectroscopy correlation.

Identifiants

pubmed: 30477741
pii: S0887-8994(18)30811-7
doi: 10.1016/j.pediatrneurol.2018.09.010
pii:
doi:

Substances chimiques

Cytokines 0
Neoplasm Proteins 0
RNA-Binding Proteins 0
small inducible cytokine subfamily E, member 1 0
Aspartic Acid 30KYC7MIAI
N-acetylaspartate 997-55-7

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

57-61

Informations de copyright

Copyright © 2018. Published by Elsevier Inc.

Auteurs

Ahmed BoAli (A)

Division of Pediatric Neurology, Department of Pediatrics, Prince Sultan Military Medical City, Riyadh, Saudi Arabia.

Kalthoum Tlili-Graiess (K)

Division of Neuroradiology, Department of Radiology, Prince Sultan Military Medical City, Riyadh, Saudi Arabia.

Amal AlHashem (A)

Division of Genetics, Department of Pediatrics, Prince Sultan Military Medical City, Riyadh, Saudi Arabia.

Saad AlShahwan (S)

Division of Pediatric Neurology, Department of Pediatrics, Prince Sultan Military Medical City, Riyadh, Saudi Arabia.

Giulio Zuccoli (G)

Division of Neuroradiology, Department of Radiology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.

Brahim Tabarki (B)

Division of Pediatric Neurology, Department of Pediatrics, Prince Sultan Military Medical City, Riyadh, Saudi Arabia. Electronic address: btabarki@hotmail.com.

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