Non-coding repeat analyses in patients with Parkinson’s disease

IntroductionThe genetic etiology of Parkinson’s disease (PD) is complex; approximately 10% of patients with PD have various gene mutations that lead to familial forms of the disease. Recent analyses of non-coding repeat regions revealed that many neurodegenerative diseases are associated with pathol...

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Main Authors: Makito Hirano, Makoto Samukawa, Satoko Miyatake, Yuko Yamagishi, Chiharu Isono, Rino Yoshikawa, Kazumasa Saigoh, Atsushi Terayama, Yuji Higashimoto, Eriko Koshimizu, Takeshi Mizuguchi, Kanako Fujii, Yoshiyuki Mitsui, Naomichi Matsumoto, Yoshitaka Nagai
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Language:English
Published: Frontiers Media S.A. 2025-07-01
Series:Frontiers in Neurology
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Online Access:https://www.frontiersin.org/articles/10.3389/fneur.2025.1606305/full
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author Makito Hirano
Makoto Samukawa
Satoko Miyatake
Satoko Miyatake
Yuko Yamagishi
Chiharu Isono
Rino Yoshikawa
Kazumasa Saigoh
Atsushi Terayama
Yuji Higashimoto
Eriko Koshimizu
Takeshi Mizuguchi
Kanako Fujii
Yoshiyuki Mitsui
Naomichi Matsumoto
Naomichi Matsumoto
Naomichi Matsumoto
Yoshitaka Nagai
author_facet Makito Hirano
Makoto Samukawa
Satoko Miyatake
Satoko Miyatake
Yuko Yamagishi
Chiharu Isono
Rino Yoshikawa
Kazumasa Saigoh
Atsushi Terayama
Yuji Higashimoto
Eriko Koshimizu
Takeshi Mizuguchi
Kanako Fujii
Yoshiyuki Mitsui
Naomichi Matsumoto
Naomichi Matsumoto
Naomichi Matsumoto
Yoshitaka Nagai
author_sort Makito Hirano
collection DOAJ
description IntroductionThe genetic etiology of Parkinson’s disease (PD) is complex; approximately 10% of patients with PD have various gene mutations that lead to familial forms of the disease. Recent analyses of non-coding repeat regions revealed that many neurodegenerative diseases are associated with pathological expansions. We evaluated the genetic background of non-coding repeat expansions in Japanese patients with PD.MethodsWe collected blood samples from 203 Japanese patients with PD and analyzed various non-coding repeat genes, including ATXN8OS, RFC1, C9ORF72, NOTCH2NLC, BEAN1/TK2, and NOP56, using PCR-Sanger sequencing, repeat-primed PCR assay, and long-read sequencing.ResultsThree patients with PD (1.5%) were found to have heterozygous repeat expansions in ATXN8OS, the gene causative of spinocerebellar ataxia type 8 and is associated with long non-coding RNA. One (0.5%) patient had compound heterozygous repeat expansions (AAGGG and ACAGG) in RFC1, the gene causative of cerebellar ataxia, neuropathy, and vestibular areflexia syndrome, which encodes a DNA repair protein. No patient had repeat expansions in C9ORF72, NOTCH2NLC, BEAN1/TK2, or NOP56. All patients with ATXN8OS repeat expansions exhibited typical parkinsonism with relatively rare subjective dysphagia, which was confirmed by videofluoroscopic results. Functional imaging, such as dopamine-transporter single photon emission computed tomography, showed abnormal findings in patients with non-coding repeat expansions.DiscussionOur findings revealed the importance of non-coding repeat expansions in Japanese patients with PD. This is the first study to show the positive result of non-coding repeat expansions in many patients with PD in Japan.
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spelling doaj-art-855c15f2a00c4f1bbfeb483374f8f29d2025-08-20T03:12:38ZengFrontiers Media S.A.Frontiers in Neurology1664-22952025-07-011610.3389/fneur.2025.16063051606305Non-coding repeat analyses in patients with Parkinson’s diseaseMakito Hirano0Makoto Samukawa1Satoko Miyatake2Satoko Miyatake3Yuko Yamagishi4Chiharu Isono5Rino Yoshikawa6Kazumasa Saigoh7Atsushi Terayama8Yuji Higashimoto9Eriko Koshimizu10Takeshi Mizuguchi11Kanako Fujii12Yoshiyuki Mitsui13Naomichi Matsumoto14Naomichi Matsumoto15Naomichi Matsumoto16Yoshitaka Nagai17Department of Neurology, Kindai University Faculty of Medicine, Osaka, JapanDepartment of Neurology, Kindai University Faculty of Medicine, Osaka, JapanDepartment of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, JapanDepartment of Clinical Genetics, Yokohama City University Hospital, Yokohama, JapanDepartment of Neurology, Kindai University Faculty of Medicine, Osaka, JapanDivision of Rehabilitation Medicine, Kindai University Hospital, Osakasayama, JapanDepartment of Neurology, Kindai University Faculty of Medicine, Osaka, JapanDepartment of Neurology, Kindai University Faculty of Medicine, Osaka, JapanDepartment of Neurology, Kindai University Faculty of Medicine, Osaka, JapanDepartment of Rehabilitation Medicine, Kindai University Faculty of Medicine, Osakasayama, JapanDepartment of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, JapanDepartment of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, JapanDepartment of Neurology, Kindai University Faculty of Medicine, Osaka, JapanDepartment of Neurology, Kindai University Faculty of Medicine, Osaka, JapanDepartment of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, JapanDepartment of Clinical Genetics, Yokohama City University Hospital, Yokohama, JapanDepartment of Rare Disease Genomics, Yokohama City University Hospital, Yokohama, JapanDepartment of Neurology, Kindai University Faculty of Medicine, Osaka, JapanIntroductionThe genetic etiology of Parkinson’s disease (PD) is complex; approximately 10% of patients with PD have various gene mutations that lead to familial forms of the disease. Recent analyses of non-coding repeat regions revealed that many neurodegenerative diseases are associated with pathological expansions. We evaluated the genetic background of non-coding repeat expansions in Japanese patients with PD.MethodsWe collected blood samples from 203 Japanese patients with PD and analyzed various non-coding repeat genes, including ATXN8OS, RFC1, C9ORF72, NOTCH2NLC, BEAN1/TK2, and NOP56, using PCR-Sanger sequencing, repeat-primed PCR assay, and long-read sequencing.ResultsThree patients with PD (1.5%) were found to have heterozygous repeat expansions in ATXN8OS, the gene causative of spinocerebellar ataxia type 8 and is associated with long non-coding RNA. One (0.5%) patient had compound heterozygous repeat expansions (AAGGG and ACAGG) in RFC1, the gene causative of cerebellar ataxia, neuropathy, and vestibular areflexia syndrome, which encodes a DNA repair protein. No patient had repeat expansions in C9ORF72, NOTCH2NLC, BEAN1/TK2, or NOP56. All patients with ATXN8OS repeat expansions exhibited typical parkinsonism with relatively rare subjective dysphagia, which was confirmed by videofluoroscopic results. Functional imaging, such as dopamine-transporter single photon emission computed tomography, showed abnormal findings in patients with non-coding repeat expansions.DiscussionOur findings revealed the importance of non-coding repeat expansions in Japanese patients with PD. This is the first study to show the positive result of non-coding repeat expansions in many patients with PD in Japan.https://www.frontiersin.org/articles/10.3389/fneur.2025.1606305/fullspinocerebellar ataxia type 8repeat diseaseparkinsonismCanvasRFC1dysphagia
spellingShingle Makito Hirano
Makoto Samukawa
Satoko Miyatake
Satoko Miyatake
Yuko Yamagishi
Chiharu Isono
Rino Yoshikawa
Kazumasa Saigoh
Atsushi Terayama
Yuji Higashimoto
Eriko Koshimizu
Takeshi Mizuguchi
Kanako Fujii
Yoshiyuki Mitsui
Naomichi Matsumoto
Naomichi Matsumoto
Naomichi Matsumoto
Yoshitaka Nagai
Non-coding repeat analyses in patients with Parkinson’s disease
Frontiers in Neurology
spinocerebellar ataxia type 8
repeat disease
parkinsonism
Canvas
RFC1
dysphagia
title Non-coding repeat analyses in patients with Parkinson’s disease
title_full Non-coding repeat analyses in patients with Parkinson’s disease
title_fullStr Non-coding repeat analyses in patients with Parkinson’s disease
title_full_unstemmed Non-coding repeat analyses in patients with Parkinson’s disease
title_short Non-coding repeat analyses in patients with Parkinson’s disease
title_sort non coding repeat analyses in patients with parkinson s disease
topic spinocerebellar ataxia type 8
repeat disease
parkinsonism
Canvas
RFC1
dysphagia
url https://www.frontiersin.org/articles/10.3389/fneur.2025.1606305/full
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