Pathological mechanisms and treatment of sporadic Parkinson’s disease: past, present, and future

Mochizuki, Hideki

doi:https://doi.org/10.1007/s00702-024-02788-w

Pathological mechanisms and treatment of sporadic Parkinson’s disease: past, present, and future

Mochizuki, Hideki

Journal of Neural Transmission, 2024, 131, 597-607

アクセス数:66件（2025-05-22 02:47 集計）

固定URL: https://hdl.handle.net/11094/97123

閲覧可能ファイル

ファイル	フォーマット	利用条件	サイズ	閲覧回数	利用開始日	説明	information
JNeuralTransm_131_597	pdf	なし	614 KB	57	2024.07.05

Creative Commons : 表示

論文情報

ファイル出力 EndNote Basic出力 Mendeley出力

タイトル	Pathological mechanisms and treatment of sporadic Parkinson’s disease: past, present, and future
著者	NRID 1000090230044 1000090230044 ORCID 0000-0002-0874-7542 0000-0002-0874-7542 researchmap permalink read0207787 read0207787 Scopus Author ID 7202006099 7202006099 著者名 Mochizuki, Hideki
キーワード等	Antisense oligonucleotide
	Apoptosis
	Iron
	Mitochondria
	Parkinson’s disease
	α-Synuclein
内容	The version of record of this article, first published in Journal of Neural Transmission, is available online at Publisher’s website: https://doi.org/10.1007/s00702-024-02788-w.
抄録	For a special issue, we review studies on the pathogenesis of nigral cell death and the treatment of sporadic Parkinson’s disease (sPD) over the past few decades, with a focus on the studies performed by Prof. Mizuno and our group. Prof. Mizuno proposed the initial concept that mitochondrial function may be impaired in sPD. When working at Jichi Medical School, he found a decrease in complex I of the mitochondrial electron transfer complex in the substantia nigra of patients with Parkinson’s disease (PD) and MPTP models. After moving to Juntendo University as a professor and chairman, he continued to study the mechanisms of cell death in the substantia nigra of patients with sPD. Under his supervision, I studied the relationships between PD and apoptosis, PD and iron involvement, mitochondrial dysfunction and apoptosis, and PD and neuroinflammation. Moving to Kitasato University, we focused on PD and the cytotoxicity of alpha synuclein (αSyn) as well as brain neuropathology. Eventually, I moved to Osaka University, where I continued working on PD and αSyn projects to promote therapeutic research. In this paper, we present the details of these studies in the following order: past, present, and future.
出版者	Springer
収録物名	Journal of Neural Transmission
巻(号)	131
ページ	597-607
刊行年月	2024-06-12
言語	英語
ハンドルURL	https://hdl.handle.net/11094/97123
PISSN	03009564
eISSN	14351463
関連情報 (isIdenticalTo)	DOI (出版社版) https://doi.org/10.1007/s00702-024-02788-w
アクセス権	open access
権利情報	This article is licensed under a Creative Commons Attribution 4.0 International License.
出版タイプ	Version of Record
カテゴリ	学術雑誌論文 Journal Article

資源タイプ	学術雑誌論文
ローカル資源タイプ	学術雑誌論文
DCTERMS.bibliographicCitation	Journal of Neural Transmission. 2024, 131, p. 597-607
DC.title	Pathological mechanisms and treatment of sporadic Parkinson’s disease: past, present, and future
DC.creator	Mochizuki, Hideki
DC.publisher	Springer
DC.language' scheme='DCTERMS.RFC1766	英語
DCTERMS.issued' scheme='DCTERMS.W3CDTF	2024-06-12
DC.identifier	https://doi.org/10.1007/s00702-024-02788-w
DC.subject	Antisense oligonucleotide
	Apoptosis
	Iron
	Mitochondria
	Parkinson’s disease
	α-Synuclein
DC.description	The version of record of this article, first published in Journal of Neural Transmission, is available online at Publisher’s website: https://doi.org/10.1007/s00702-024-02788-w.
DCTERMS.abstract	For a special issue, we review studies on the pathogenesis of nigral cell death and the treatment of sporadic Parkinson’s disease (sPD) over the past few decades, with a focus on the studies performed by Prof. Mizuno and our group. Prof. Mizuno proposed the initial concept that mitochondrial function may be impaired in sPD. When working at Jichi Medical School, he found a decrease in complex I of the mitochondrial electron transfer complex in the substantia nigra of patients with Parkinson’s disease (PD) and MPTP models. After moving to Juntendo University as a professor and chairman, he continued to study the mechanisms of cell death in the substantia nigra of patients with sPD. Under his supervision, I studied the relationships between PD and apoptosis, PD and iron involvement, mitochondrial dysfunction and apoptosis, and PD and neuroinflammation. Moving to Kitasato University, we focused on PD and the cytotoxicity of alpha synuclein (αSyn) as well as brain neuropathology. Eventually, I moved to Osaka University, where I continued working on PD and αSyn projects to promote therapeutic research. In this paper, we present the details of these studies in the following order: past, present, and future.
DC.rights	This article is licensed under a Creative Commons Attribution 4.0 International License.
DC.format	97123
citation_title	Pathological mechanisms and treatment of sporadic Parkinson’s disease: past, present, and future
citation_author	Mochizuki, Hideki
citation_publisher	Springer
citation_language	英語
citation_date	2024-06-12
citation_journal_title	Journal of Neural Transmission
citation_volume	131
citation_firstpage	597
citation_lastpage	607
citation_doi	https://doi.org/10.1007/s00702-024-02788-w
citation_public_url	https://hdl.handle.net/11094/97123

Pathological mechanisms and treatment of sporadic Parkinson’s disease: past, present, and future

閲覧可能ファイル

論文情報

論文詳細を表示