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

dc.contributor.coauthorTuray, Sevim
dc.contributor.coauthorEroz, Recep
dc.contributor.departmentKUTTAM (Koç University Research Center for Translational Medicine)
dc.contributor.departmentSchool of Medicine
dc.contributor.departmentNDAL (Neurodegeneration Research Laboratory)
dc.contributor.facultymemberYes
dc.contributor.kuauthorBaşak, Ayşe Nazlı
dc.contributor.schoolcollegeinstituteResearch Center
dc.contributor.schoolcollegeinstituteSCHOOL OF MEDICINE
dc.contributor.schoolcollegeinstituteLaboratory
dc.date.accessioned2024-11-09T23:58:24Z
dc.date.issued2021
dc.description.abstractChildhood-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.
dc.description.fulltextNo
dc.description.harvestedfromManual
dc.description.indexedbyWOS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.openaccessNO
dc.description.peerreviewstatusN/A
dc.description.publisherscopeInternational
dc.description.readpublishN/A
dc.description.sponsoredbyTubitakEuN/A
dc.description.sponsorshipSuna and İnan Kıraç Foundation
dc.description.sponsorshipKoç University School of Medicine
dc.description.studentonlypublicationNo
dc.description.studentpublicationNo
dc.description.versionN/A
dc.identifier.WoSQuartileQ4
dc.identifier.doi10.1007/s10048-021-00643-8
dc.identifier.eissn1364-6753
dc.identifier.embargoN/A
dc.identifier.endpage132
dc.identifier.issn1364-6745
dc.identifier.issue2
dc.identifier.pubmed33909173
dc.identifier.scopus2-s2.0-85105413051
dc.identifier.startpage127
dc.identifier.urihttps://doi.org/10.1007/s10048-021-00643-8
dc.identifier.urihttps://hdl.handle.net/20.500.14288/15463
dc.identifier.volume22
dc.identifier.wos000645164200001
dc.keywordsAGTPBP1-related neurodegeneration
dc.keywordsAGTPBP1 gene
dc.keywordsHypotonia
dc.keywordsMotor and cognitive retardation
dc.language.isoeng
dc.publisherSpringer
dc.relation.affiliationKoç University
dc.relation.collectionKoç University Institutional Repository
dc.relation.ispartofNeurogenetics
dc.relation.openaccessN/A
dc.rightsN/A
dc.subjectGenetics
dc.subjectHeredity
dc.subjectClinical neurology
dc.titleA novel pathogenic variant in the 3ʹ end of the AGTPBP1 gene gives rise to neurodegeneration without cerebellar atrophy: an expansion of the disease phenotype?
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.kuauthorBaşak, Ayşe Nazlı
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