M
Makoto Naoi
Researcher at Nagoya Institute of Technology
Publications - 197
Citations - 6897
Makoto Naoi is an academic researcher from Nagoya Institute of Technology. The author has contributed to research in topics: Dopamine & Dopaminergic. The author has an hindex of 46, co-authored 196 publications receiving 6704 citations. Previous affiliations of Makoto Naoi include Nagoya City University & Nagoya University.
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Striatal dopamine turnover during treadmill running in the rat: Relation to the speed of running
TL;DR: Data suggest that both the synthesis and metabolism of DA have a close relationship with physical exercise and might contribute to adjusting extracellular DA levels within an adequate range in response to exercise intensity.
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Gene therapy for mitochondrial disease by delivering restriction endonuclease SmaI into mitochondria.
Masashi Tanaka,Harm-Jan Borgeld,Jin Zhang,Shin-ichi Muramatsu,Jian-Sheng Gong,Makoto Yoneda,Wakako Maruyama,Makoto Naoi,Tohru Ibi,Ko Sahashi,Masayo Shamoto,Noriyuki Fuku,Miyuki Kurata,Yoshiji Yamada,Kumi Nishizawa,Yukihiro Akao,Nobuko Ohishi,Shigeaki Miyabayashi,Hiraku Umemoto,Tatsuo Muramatsu,Koichi Furukawa,Akihiko Kikuchi,Imaharu Nakano,Keiya Ozawa,Kunio Yagi +24 more
TL;DR: It is demonstrated that mitochondria targeted by the SmaI enzyme showed specific elimination of the mutant mtDNA, resulting in restoration of both the normal intracellular ATP level and normal mitochondrial membrane potential.
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Hydroxyl radical formation in diabetic rats induced by streptozotocin.
TL;DR: Production of hydroxyl radicals was examined in the diabetic rats induced by streptozotocin to prove its involvement to the pathogenesis of diabetes and 2,3-dihydroxybenzoic acid was suggested to account for some pathological process especially in the heart muscle and brain.
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Transfection-enforced Bcl-2 overexpression and an anti-Parkinson drug, rasagiline, prevent nuclear accumulation of glyceraldehyde-3-phosphate dehydrogenase induced by an endogenous dopaminergic neurotoxin, N-methyl(R)salsolinol.
TL;DR: The results suggest that GAPDH may accumulate in nuclei as a consequence of signal transduction, which is antagonized by anti‐apoptotic Bcl‐2 protein family and rasagiline.
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Mitochondrial permeability transition mediates apoptosis induced by N-methyl(R)salsolinol, an endogenous neurotoxin, and is inhibited by Bcl-2 and rasagiline, N-propargyl-1(R)-aminoindan.
Yukihiro Akao,Wakako Maruyama,Shigeomi Shimizu,Hong Yi,Yoshihito Nakagawa,Masayo Shamoto-Nagai,Moussa B.H. Youdim,Yoshihide Tsujimoto,Makoto Naoi +8 more
TL;DR: Rasagiline, N‐propargyl‐1(R)‐aminoindan, which is a now under a clinical trial for Parkinson's disease, suppressed the ΔΨm reduction, release of cytochrome c, and apoptosis induced by NM(R),Sal in SH‐SY5Y cells, proving that rasagILine directly targets the mitochondria also.