A novel POLR3A genotype leads to leukodystrophy type-7 in two siblings with unusually late age of onset.


Journal

BMC neurology
ISSN: 1471-2377
Titre abrégé: BMC Neurol
Pays: England
ID NLM: 100968555

Informations de publication

Date de publication:
29 Jun 2020
Historique:
received: 19 03 2020
accepted: 19 06 2020
entrez: 1 7 2020
pubmed: 1 7 2020
medline: 24 10 2020
Statut: epublish

Résumé

Leukodystrophies are familial heterogeneous disorders primarily affecting the white matter, which are defined as hypomyelinating or demyelinating based on disease severity as assessed at MRI. Recently, a group of clinically overlapping hypomyelinating leukodystrophies (HL) has been associated with mutations in RNA polymerase III enzymes (Pol III) subunits. In this manuscript, we describe two Italian siblings carrying a novel POLR3A genotype. MRI imaging, genetic analysis, and clinical data led to diagnosing HL type 7. The female sibling, at the age of 34, is tetra-paretic and suffers from severe cognitive regression. She had a disease onset at the age of 19, characterized by slow and progressive cognitive impairment associated with gait disturbances and amenorrhea. The male sibling was diagnosed during an MRI carried out for cephalalgia at the age of 41. After 5 years, he developed mild cognitive impairment, dystonia with 4-limb hypotonia, and moderate dysmetria with balance and gait impairment. The present study provides the first evidence of unusually late age of onset in HL, describing two siblings with a novel POLR3A genotype which showed the first symptoms at the age of 41 and 19, respectively. This provides a powerful insight into clinical heterogeneity and genotype-phenotype correlation in POLR3A related HL.

Sections du résumé

BACKGROUND BACKGROUND
Leukodystrophies are familial heterogeneous disorders primarily affecting the white matter, which are defined as hypomyelinating or demyelinating based on disease severity as assessed at MRI. Recently, a group of clinically overlapping hypomyelinating leukodystrophies (HL) has been associated with mutations in RNA polymerase III enzymes (Pol III) subunits.
CASE PRESENTATION METHODS
In this manuscript, we describe two Italian siblings carrying a novel POLR3A genotype. MRI imaging, genetic analysis, and clinical data led to diagnosing HL type 7. The female sibling, at the age of 34, is tetra-paretic and suffers from severe cognitive regression. She had a disease onset at the age of 19, characterized by slow and progressive cognitive impairment associated with gait disturbances and amenorrhea. The male sibling was diagnosed during an MRI carried out for cephalalgia at the age of 41. After 5 years, he developed mild cognitive impairment, dystonia with 4-limb hypotonia, and moderate dysmetria with balance and gait impairment.
CONCLUSIONS CONCLUSIONS
The present study provides the first evidence of unusually late age of onset in HL, describing two siblings with a novel POLR3A genotype which showed the first symptoms at the age of 41 and 19, respectively. This provides a powerful insight into clinical heterogeneity and genotype-phenotype correlation in POLR3A related HL.

Identifiants

pubmed: 32600288
doi: 10.1186/s12883-020-01835-9
pii: 10.1186/s12883-020-01835-9
pmc: PMC7322863
doi:

Substances chimiques

POLR3A protein, human EC 2.7.7.6
RNA Polymerase III EC 2.7.7.6

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

258

Subventions

Organisme : Ministero della Salute (IT)
ID : Partially Supported By Ministry Of Health (Current Research 2019-2023- Principal Investigator: Identification Of New Variants And / Or New Genes Responsible For Ataxia And Spastic Paraplegia)

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Auteurs

Rosa Campopiano (R)

I.R.C.C.S. I.N.M. Neuromed, via Atinense 18, 86077, Pozzilli, Italy.

Rosangela Ferese (R)

I.R.C.C.S. I.N.M. Neuromed, via Atinense 18, 86077, Pozzilli, Italy.

Stefania Zampatti (S)

Molecular Genetics Laboratory UILDM, Santa Lucia Foundation IRCCS, Rome, Italy.

Emiliano Giardina (E)

Molecular Genetics Laboratory UILDM, Santa Lucia Foundation IRCCS, Rome, Italy.
Department of Biomedicine and Prevention, University of Rome "Tor Vergata", Rome, Italy.

Francesca Biagioni (F)

I.R.C.C.S. I.N.M. Neuromed, via Atinense 18, 86077, Pozzilli, Italy.

Claudio Colonnese (C)

I.R.C.C.S. I.N.M. Neuromed, via Atinense 18, 86077, Pozzilli, Italy.

Diego Centonze (D)

I.R.C.C.S. I.N.M. Neuromed, via Atinense 18, 86077, Pozzilli, Italy.
Dipartimento di Medicina dei Sistemi, Università di Roma Tor Vergata, Rome, Italy.

Marianna Storto (M)

I.R.C.C.S. I.N.M. Neuromed, via Atinense 18, 86077, Pozzilli, Italy.

Fabio Buttari (F)

I.R.C.C.S. I.N.M. Neuromed, via Atinense 18, 86077, Pozzilli, Italy.

Edoardo Fraviga (E)

Stem Cell and Neurogenesis Unit, Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.

Vania Broccoli (V)

Stem Cell and Neurogenesis Unit, Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy.
CNR Institute of Neuroscience, Milan, Italy.

Mirco Fanelli (M)

Department of Biomolecular Sciences, University of Urbino "Carlo Bo", Urbino, Italy.

Francesco Fornai (F)

I.R.C.C.S. I.N.M. Neuromed, via Atinense 18, 86077, Pozzilli, Italy.
Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy.

Stefano Gambardella (S)

I.R.C.C.S. I.N.M. Neuromed, via Atinense 18, 86077, Pozzilli, Italy. stefano.gambardella@uniurb.it.
Department of Biomolecular Sciences, University of Urbino "Carlo Bo", Urbino, Italy. stefano.gambardella@uniurb.it.

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