Neuropathologically directed profiling of PRNP somatic and germline variants in sporadic human prion disease.


Journal

Acta neuropathologica
ISSN: 1432-0533
Titre abrégé: Acta Neuropathol
Pays: Germany
ID NLM: 0412041

Informations de publication

Date de publication:
24 Jul 2024
Historique:
received: 21 06 2024
accepted: 20 07 2024
revised: 19 07 2024
medline: 26 7 2024
pubmed: 26 7 2024
entrez: 24 7 2024
Statut: epublish

Résumé

Creutzfeldt-Jakob Disease (CJD), the most common human prion disease, is associated with pathologic misfolding of the prion protein (PrP), encoded by the PRNP gene. Of human prion disease cases, < 1% were transmitted by misfolded PrP, ~ 15% are inherited, and ~ 85% are sporadic (sCJD). While familial cases are inherited through germline mutations in PRNP, the cause of sCJD is unknown. Somatic mutations have been hypothesized as a cause of sCJD, and recent studies have revealed that somatic mutations accumulate in neurons during aging. To investigate the hypothesis that somatic mutations in PRNP may underlie sCJD, we performed deep DNA sequencing of PRNP in 205 sCJD cases and 170 age-matched non-disease controls. We included 5 cases of Heidenhain variant sporadic CJD (H-sCJD), where visual symptomatology and neuropathology implicate localized initiation of prion formation, and examined multiple regions across the brain including in the affected occipital cortex. We employed Multiple Independent Primer PCR Sequencing (MIPP-Seq) with a median depth of > 5000× across the PRNP coding region and analyzed for variants using MosaicHunter. An allele mixing experiment showed positive detection of variants in bulk DNA at a variant allele fraction (VAF) as low as 0.2%. We observed multiple polymorphic germline variants among individuals in our cohort. However, we did not identify bona fide somatic variants in sCJD, including across multiple affected regions in H-sCJD, nor in control individuals. Beyond our stringent variant-identification pipeline, we also analyzed VAFs from raw sequencing data, and observed no evidence of prion disease enrichment for the known germline pathogenic variants P102L, D178N, and E200K. The lack of PRNP pathogenic somatic mutations in H-sCJD or the broader cohort of sCJD suggests that clonal somatic mutations may not play a major role in sporadic prion disease. With H-sCJD representing a localized presentation of neurodegeneration, this serves as a test of the potential role of clonal somatic mutations in genes known to cause familial neurodegeneration.

Identifiants

pubmed: 39048735
doi: 10.1007/s00401-024-02774-2
pii: 10.1007/s00401-024-02774-2
doi:

Substances chimiques

Prion Proteins 0
PRNP protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

10

Subventions

Organisme : NCEZID CDC HHS
ID : CK000309
Pays : United States
Organisme : NINDS NIH HHS
ID : NS074317
Pays : United States
Organisme : NINDS NIH HHS
ID : NS103848
Pays : United States
Organisme : NIA NIH HHS
ID : AG086138
Pays : United States
Organisme : NIA NIH HHS
ID : AG082346
Pays : United States
Organisme : NIA NIH HHS
ID : AG065502
Pays : United States
Organisme : NIA NIH HHS
ID : HL007627
Pays : United States
Organisme : NIA NIH HHS
ID : AG079857
Pays : United States
Organisme : Doris Duke Charitable Foundation
ID : 2021183
Pays : United States
Organisme : BrightFocus Foundation
ID : A20201292F

Informations de copyright

© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

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Auteurs

Gannon A McDonough (GA)

Division of Neuropathology, Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA.

Yuchen Cheng (Y)

Division of Genetics and Genomics, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA.
Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA.

Katherine S Morillo (KS)

Division of Genetics and Genomics, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA.

Ryan N Doan (RN)

Division of Genetics and Genomics, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA.
Harvard Medical School, Boston, MA, USA.

Zinan Zhou (Z)

Division of Genetics and Genomics, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA.

Connor J Kenny (CJ)

Division of Genetics and Genomics, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA.

Aaron Foutz (A)

Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.

Chae Kim (C)

Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Department of Neurology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.

Mark L Cohen (ML)

Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Department of Neurology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
National Prion Disease Pathology Surveillance Center, Case Western Reserve University School of Medicine, Cleveland, OH, USA.

Brian S Appleby (BS)

Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Department of Neurology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
National Prion Disease Pathology Surveillance Center, Case Western Reserve University School of Medicine, Cleveland, OH, USA.

Christopher A Walsh (CA)

Division of Genetics and Genomics, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA.
Harvard Medical School, Boston, MA, USA.
Howard Hughes Medical Institute, Boston, MA, USA.

Jiri G Safar (JG)

Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Department of Neurology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA.

August Yue Huang (AY)

Division of Genetics and Genomics, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA. yue.huang@childrens.harvard.edu.
Harvard Medical School, Boston, MA, USA. yue.huang@childrens.harvard.edu.

Michael B Miller (MB)

Division of Neuropathology, Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA. mbmiller@bwh.harvard.edu.
Division of Genetics and Genomics, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA. mbmiller@bwh.harvard.edu.
Harvard Medical School, Boston, MA, USA. mbmiller@bwh.harvard.edu.

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