Clinical and Molecular Characterization of a Novel Progranulin Deletion Associated with Different Phenotypes.


Journal

Journal of Alzheimer's disease : JAD
ISSN: 1875-8908
Titre abrégé: J Alzheimers Dis
Pays: Netherlands
ID NLM: 9814863

Informations de publication

Date de publication:
2020
Historique:
pubmed: 1 6 2020
medline: 8 5 2021
entrez: 1 6 2020
Statut: ppublish

Résumé

Mutations in the GRN gene are causative for an autosomal dominant form of frontotemporal dementia. The objective of the present study is to describe clinical and molecular features of three siblings harboring the GRN deletion NM_002087.3:c.295_308delTGCCCACGGGGCTT, p.(Cys99Profs*15) identified with next generation sequencing. Our patients demonstrated heterogeneous clinical phenotypes, such as progressive supranuclear palsy-like in the proband and the behavioral variant of frontotemporal dementia in the two affected siblings. Progranulin haploinsufficiency was revealed by both gene expression and protein analyses. The pathogenicity of the novel GRN deletion c.295_308del TGCCCACGGGGCTT is confirmed by both functional analysis and segregation in three affected siblings.

Sections du résumé

BACKGROUND
Mutations in the GRN gene are causative for an autosomal dominant form of frontotemporal dementia.
OBJECTIVE/METHODS
The objective of the present study is to describe clinical and molecular features of three siblings harboring the GRN deletion NM_002087.3:c.295_308delTGCCCACGGGGCTT, p.(Cys99Profs*15) identified with next generation sequencing.
RESULTS
Our patients demonstrated heterogeneous clinical phenotypes, such as progressive supranuclear palsy-like in the proband and the behavioral variant of frontotemporal dementia in the two affected siblings. Progranulin haploinsufficiency was revealed by both gene expression and protein analyses.
CONCLUSION
The pathogenicity of the novel GRN deletion c.295_308del TGCCCACGGGGCTT is confirmed by both functional analysis and segregation in three affected siblings.

Identifiants

pubmed: 32474471
pii: JAD200151
doi: 10.3233/JAD-200151
doi:

Substances chimiques

GRN protein, human 0
Progranulins 0

Types de publication

Case Reports Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

341-347

Auteurs

Marina Picillo (M)

Center for Neurodegenerative Diseases (CEMAND); Department of Medicine, Surgery and Dentistry, Neuroscience Section, University of Salerno, Italy.

Emilia Vitale (E)

Institute of Biochemistry and Cell Biology (IBBC), CNR, Naples, Italy.

Antonella Rendina (A)

Institute of Biochemistry and Cell Biology (IBBC), CNR, Naples, Italy.

Aldo Donizetti (A)

Department of Biology, University of Naples Federico II, Naples, Italy.

Vincenza Aliperti (V)

Department of Biology, University of Naples Federico II, Naples, Italy.

Maria Francesca Tepedino (MF)

Center for Neurodegenerative Diseases (CEMAND); Department of Medicine, Surgery and Dentistry, Neuroscience Section, University of Salerno, Italy.

Giovanna Dati (G)

Center for Neurodegenerative Diseases (CEMAND); Department of Medicine, Surgery and Dentistry, Neuroscience Section, University of Salerno, Italy.

Monia Ginevrino (M)

Istituto di Medicina Genomica, Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Roma, Italia.

Enza Maria Valente (EM)

Department of Molecular Medicine, University of Pavia, Pavia, Italy.
IRCCS Mondino Foundation, Pavia, Italy.

Paolo Barone (P)

Center for Neurodegenerative Diseases (CEMAND); Department of Medicine, Surgery and Dentistry, Neuroscience Section, University of Salerno, Italy.

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Classifications MeSH