Association of biallelic RFC1 expansion with early-onset Parkinson's disease.


Journal

European journal of neurology
ISSN: 1468-1331
Titre abrégé: Eur J Neurol
Pays: England
ID NLM: 9506311

Informations de publication

Date de publication:
05 2023
Historique:
revised: 19 01 2023
received: 22 12 2022
accepted: 23 01 2023
medline: 6 4 2023
pubmed: 28 1 2023
entrez: 27 1 2023
Statut: ppublish

Résumé

The biallelic repeat expansion (AAGGG) A nationwide cohort of 273 Finnish patients with early-onset PD was examined for the biallelic intronic expansion in RFC1. The expansion (AAGGG) Three patients were found with the biallelic (AAGGG) Our results suggest that (AAGGG)

Sections du résumé

BACKGROUND AND PURPOSE
The biallelic repeat expansion (AAGGG)
METHODS
A nationwide cohort of 273 Finnish patients with early-onset PD was examined for the biallelic intronic expansion in RFC1. The expansion (AAGGG)
RESULTS
Three patients were found with the biallelic (AAGGG)
CONCLUSIONS
Our results suggest that (AAGGG)

Identifiants

pubmed: 36705320
doi: 10.1111/ene.15717
doi:

Substances chimiques

RFC1 protein, human 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1256-1261

Informations de copyright

© 2023 The Authors. European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.

Références

Blauwendraat C, Nalls MA, Singleton AB. The genetic architecture of Parkinson's disease. Lancet Neurol. 2020;19:170-178.
Cortese A, Simone R, Sullivan R, et al. Biallelic expansion of an intronic repeat in RFC1 is a common cause of late-onset ataxia. Nat Genet. 2019;51:649-658.
Rafehi H, Szmulewicz DJ, Bennett MF, et al. Bioinformatics-based identification of expanded repeats: a non-reference intronic pentamer expansion in RFC1 causes CANVAS. Am J Hum Genet. 2019;105:151-165.
Traschütz A, Cortese A, Reich S, et al. Natural history, phenotypic spectrum, and discriminative features of multisystemic RFC1 disease. Neurology. 2021;96:e1369-e1382.
Korpioja A, Krüger J, Hurme-Niiranen A, et al. Cognitive impairment is not uncommon in patients with biallelic RFC1 AAGGG repeat expansion, but the expansion is rare in patients with cognitive disease. Parkinsonism Relat Disord. 2022;103:98-101.
Matos PCAAP, Rezende TJR, Schmitt GS, et al. Brain structural signature of RFC1-related disorder. Mov Disord. 2021;36:2634-2641.
Wan L, Chen Z, Wan N, et al. Biallelic intronic AAGGG expansion of RFC1 is related to multiple system atrophy. Ann Neurol. 2020;88:1132-1143.
Schoeberl F, Abicht A, Kuepper C, et al. Sensory neuropathy due to RFC1 in a patient with ALS: more than a coincidence? J Neurol. 2021;269:2774-2777.
Kytövuori L, Sipilä J, Doi H, et al. Biallelic expansion in RFC1 as a rare cause of Parkinson's disease. NPJ Parkinsons Dis. 2022;8:6.
Ylikotila P, Tiirikka T, Moilanen JS, Kääriäinen H, Marttila R, Majamaa K. Epidemiology of early-onset Parkinson's disease in Finland. Parkinsonism Relat Disord. 2015;21:938-942.
Siitonen A, Nalls MA, Hernández D, et al. Genetics of early-onset Parkinson's disease in Finland: exome sequencing and genome-wide association study. Neurobiol Aging. 2017;53:195-e7.
Norio R. Finnish Disease Heritage I: characteristics, causes, background. Hum Genet. 2003;112:441-456.
Marder K, Levy G, Louis ED, et al. Accuracy of family history data on Parkinson's disease. Neurology. 2003;61:18-23.
Cortese A, Tozza S, Yau WY, et al. Cerebellar ataxia, neuropathy, vestibular areflexia syndrome due to RFC1 repeat expansion. Brain. 2020;143:480-490.
Sullivan R, Yau WY, Chelban V, et al. RFC1-related ataxia is a mimic of early multiple system atrophy. J Neurol Neurosurg Psychiatry. 2021;92:444-446.
Paulson H. Chapter 9, Repeat expansion diseases. In: Geschwind DH, Paulson HL, Klein C, eds. Handbook of Clinical Neurology. Vol 147; 2018:105-123. Elsevier.

Auteurs

Pauli Ylikotila (P)

Clinical Neurosciences, University of Turku, Turku, Finland.
Neurocenter Turku University Hospital, Turku, Finland.

Jussi Sipilä (J)

Clinical Neurosciences, University of Turku, Turku, Finland.
Department of Neurology, Siun Sote North Karelia Central Hospital, Joensuu, Finland.

Tiina Alapirtti (T)

Department of Neurology, Kanta-Häme Central Hospital, Hämeenlinna, Finland.

Riitta Ahmasalo (R)

Department of Neurology, Lapland Central Hospital, Rovaniemi, Finland.

Eriko Koshimizu (E)

Department of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Satoko Miyatake (S)

Department of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Department of Clinical Genetics, Yokohama City University Hospital, Yokohama, Japan.

Anri Hurme-Niiranen (A)

Research Unit of Clinical Medicine, Medical Research Center Oulu, Oulu University Hospital, University of Oulu, Oulu, Finland.
Neurocenter, Neurology, Oulu University Hospital, Oulu, Finland.

Ari Siitonen (A)

Research Unit of Clinical Medicine, Medical Research Center Oulu, Oulu University Hospital, University of Oulu, Oulu, Finland.
Neurocenter, Neurology, Oulu University Hospital, Oulu, Finland.

Hiroshi Doi (H)

Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Fumiaki Tanaka (F)

Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Naomichi Matsumoto (N)

Department of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Kari Majamaa (K)

Research Unit of Clinical Medicine, Medical Research Center Oulu, Oulu University Hospital, University of Oulu, Oulu, Finland.
Neurocenter, Neurology, Oulu University Hospital, Oulu, Finland.

Laura Kytövuori (L)

Research Unit of Clinical Medicine, Medical Research Center Oulu, Oulu University Hospital, University of Oulu, Oulu, Finland.
Neurocenter, Neurology, Oulu University Hospital, Oulu, Finland.

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