Accelerated senescence exacerbates α-synucleinopathy in senescence-accelerated prone 8 mice via persistent neuroinflammation.

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作者： Hiroshi,Sakiyama ^[1] ; Kousuke,Baba ^[2] ; Yasuyoshi,Kimura ^[1] ; Kotaro,Ogawa ^[1] ; Ujiakira,Nishiike ^[1] ; Hideki,Hayakawa ^[1] ; Miki,Yoshida ^[1] ; Cesar,Aguirre ^[1] ; Kensuke,Ikenaka ^[1] ; Seiichi,Nagano ^[3] ; Hideki,Mochizuki ^[4]

作者单位： Department of Neurology, Osaka University, Graduate School of Medicine, Osaka, Japan. ^[1] Department of Neurology, Osaka University, Graduate School of Medicine, Osaka, Japan; Department of Neurotherapeutics, Osaka University Graduate School of Medicine, Osaka, Japan. Electronic address: babablanc@gmail.com. ^[2] Department of Neurology, Osaka University, Graduate School of Medicine, Osaka, Japan; Department of Neurotherapeutics, Osaka University Graduate School of Medicine, Osaka, Japan. ^[3] Department of Neurology, Osaka University, Graduate School of Medicine, Osaka, Japan. Electronic address: hmochizuki@neurol.med.osaka-u.ac.jp. ^[4]

关键词 CC-Chemokine ligand 21 Neuroinflammation Parkinson's disease Senescence-accelerated prone 8 (SAMP8) mice α-synucleinopathy

主题词动物(Animals);小鼠(Mice);α突触核蛋白(alpha-Synuclein);衰老(Aging);男(雄)性(Male);黑质(Substantia Nigra)

DOI 10.1016/j.neuint.2024.105906

PMID 39586378

发布时间 2025-01-10

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