Mitochondrial Serine Protease HTRA2 p.G399S in a Female with Di George Syndrome and Parkinson’s Disease

Deletion at 22q11.2 responsible for Di George syndrome (DGs) is a risk factor for early-onset Parkinson’s disease (EOPD). To date, all patients reported with 22q11.2 deletions and parkinsonian features are negative for a family history of PD, and possible mutations in PD-related genes were not prope...

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Main Authors: Stefano Gambardella, Rosangela Ferese, Simona Scala, Stefania Carboni, Francesca Biagioni, Giardina Emiliano, Stefania Zampatti, Nicola Modugno, Francesco Fabbiano, Francesco Fornai, Diego Centonze, Stefano Ruggieri
Format: Article
Language:English
Published: Wiley 2018-01-01
Series:Parkinson's Disease
Online Access:http://dx.doi.org/10.1155/2018/5651435
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author Stefano Gambardella
Rosangela Ferese
Simona Scala
Stefania Carboni
Francesca Biagioni
Giardina Emiliano
Stefania Zampatti
Nicola Modugno
Francesco Fabbiano
Francesco Fornai
Diego Centonze
Stefano Ruggieri
author_facet Stefano Gambardella
Rosangela Ferese
Simona Scala
Stefania Carboni
Francesca Biagioni
Giardina Emiliano
Stefania Zampatti
Nicola Modugno
Francesco Fabbiano
Francesco Fornai
Diego Centonze
Stefano Ruggieri
author_sort Stefano Gambardella
collection DOAJ
description Deletion at 22q11.2 responsible for Di George syndrome (DGs) is a risk factor for early-onset Parkinson’s disease (EOPD). To date, all patients reported with 22q11.2 deletions and parkinsonian features are negative for a family history of PD, and possible mutations in PD-related genes were not properly evaluated. The goal of this paper was to identify variants in PD genes that could contribute, together with 22q11.2 del, to the onset of parkinsonian features in patients affected by Di George syndrome. To this aim, sequencing analysis of 4800 genes including 17 PD-related genes was performed in a patient affected by DGs and EOPD. The analysis identified mutation p.Gly399Ser in OMI/HTRA2 (PARK13). To date, the mechanism that links DGs with parkinsonian features is poorly understood. The identification of a mutation in a PARK gene suggests that variants in PD-related genes, or in genes still not associated with PD, could contribute, together with deletion at 22q11.2, to the EOPD in patients affected by DGs. Further genetic analyses in a large number of patients are strongly required to understand this mechanism and to establish the pathogenetic role of p.Gly399Ser in OMI/HTRA2.
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issn 2090-8083
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publishDate 2018-01-01
publisher Wiley
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series Parkinson's Disease
spelling doaj-art-e030afe8d2794200a7a645bcd96743982025-08-20T02:21:28ZengWileyParkinson's Disease2090-80832042-00802018-01-01201810.1155/2018/56514355651435Mitochondrial Serine Protease HTRA2 p.G399S in a Female with Di George Syndrome and Parkinson’s DiseaseStefano Gambardella0Rosangela Ferese1Simona Scala2Stefania Carboni3Francesca Biagioni4Giardina Emiliano5Stefania Zampatti6Nicola Modugno7Francesco Fabbiano8Francesco Fornai9Diego Centonze10Stefano Ruggieri11IRCCS Neuromed, Pozzilli, ItalyIRCCS Neuromed, Pozzilli, ItalyIRCCS Neuromed, Pozzilli, ItalyMolecular Genetics Laboratory UILDM, Santa Lucia Foundation, Rome, ItalyIRCCS Neuromed, Pozzilli, ItalyMolecular Genetics Laboratory UILDM, Santa Lucia Foundation, Rome, ItalyIRCCS Neuromed, Pozzilli, ItalyIRCCS Neuromed, Pozzilli, ItalyIRCCS Neuromed, Pozzilli, ItalyIRCCS Neuromed, Pozzilli, ItalyIRCCS Neuromed, Pozzilli, ItalyIRCCS Neuromed, Pozzilli, ItalyDeletion at 22q11.2 responsible for Di George syndrome (DGs) is a risk factor for early-onset Parkinson’s disease (EOPD). To date, all patients reported with 22q11.2 deletions and parkinsonian features are negative for a family history of PD, and possible mutations in PD-related genes were not properly evaluated. The goal of this paper was to identify variants in PD genes that could contribute, together with 22q11.2 del, to the onset of parkinsonian features in patients affected by Di George syndrome. To this aim, sequencing analysis of 4800 genes including 17 PD-related genes was performed in a patient affected by DGs and EOPD. The analysis identified mutation p.Gly399Ser in OMI/HTRA2 (PARK13). To date, the mechanism that links DGs with parkinsonian features is poorly understood. The identification of a mutation in a PARK gene suggests that variants in PD-related genes, or in genes still not associated with PD, could contribute, together with deletion at 22q11.2, to the EOPD in patients affected by DGs. Further genetic analyses in a large number of patients are strongly required to understand this mechanism and to establish the pathogenetic role of p.Gly399Ser in OMI/HTRA2.http://dx.doi.org/10.1155/2018/5651435
spellingShingle Stefano Gambardella
Rosangela Ferese
Simona Scala
Stefania Carboni
Francesca Biagioni
Giardina Emiliano
Stefania Zampatti
Nicola Modugno
Francesco Fabbiano
Francesco Fornai
Diego Centonze
Stefano Ruggieri
Mitochondrial Serine Protease HTRA2 p.G399S in a Female with Di George Syndrome and Parkinson’s Disease
Parkinson's Disease
title Mitochondrial Serine Protease HTRA2 p.G399S in a Female with Di George Syndrome and Parkinson’s Disease
title_full Mitochondrial Serine Protease HTRA2 p.G399S in a Female with Di George Syndrome and Parkinson’s Disease
title_fullStr Mitochondrial Serine Protease HTRA2 p.G399S in a Female with Di George Syndrome and Parkinson’s Disease
title_full_unstemmed Mitochondrial Serine Protease HTRA2 p.G399S in a Female with Di George Syndrome and Parkinson’s Disease
title_short Mitochondrial Serine Protease HTRA2 p.G399S in a Female with Di George Syndrome and Parkinson’s Disease
title_sort mitochondrial serine protease htra2 p g399s in a female with di george syndrome and parkinson s disease
url http://dx.doi.org/10.1155/2018/5651435
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