K
Katsutoshi Furukawa
Researcher at Tohoku Pharmaceutical University
Publications - 158
Citations - 8457
Katsutoshi Furukawa is an academic researcher from Tohoku Pharmaceutical University. The author has contributed to research in topics: Dementia & Alzheimer's disease. The author has an hindex of 46, co-authored 152 publications receiving 7593 citations. Previous affiliations of Katsutoshi Furukawa include National Institutes of Health & Tohoku University.
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Journal ArticleDOI
Tumor necrosis factors alpha and beta protect neurons against amyloid beta-peptide toxicity: evidence for involvement of a kappa B-binding factor and attenuation of peroxide and Ca2+ accumulation
Steven W. Barger,Dorothee Hörster,Katsutoshi Furukawa,Yadong Goodman,Josef Krieglstein,Mark P. Mattson +5 more
TL;DR: Data suggest that TNFs protect hippocampal neurons against A beta toxicity by suppressing accumulation of ROS and Ca2+ and that kappa B-dependent transcription is sufficient to mediate these effects.
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Selective butyrylcholinesterase inhibition elevates brain acetylcholine, augments learning and lowers Alzheimer β-amyloid peptide in rodent
Nigel H. Greig,Tadanobu Utsuki,Tadanobu Utsuki,Donald K. Ingram,Yue Wang,Giancarlo Pepeu,Carla Scali,Qian Sheng Yu,Jacek Mamczarz,Harold W. Holloway,Tony Giordano,Demao Chen,Katsutoshi Furukawa,Kumar Sambamurti,Arnold Brossi,Debomoy K. Lahiri +15 more
TL;DR: In rats, cymserine analogs caused long-term inhibition of brain BChE and elevated extracellular ACh levels, without inhibitory effects on acetylcholinesterase, and improved the cognitive performance of aged rats.
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Neurotrophic factors attenuate glutamate-induced accumulation of peroxides, elevation of intracellular Ca2+ concentration, and neurotoxicity and increase antioxidant enzyme activities in hippocampal neurons.
TL;DR: The data suggest that glutamate toxicity involves peroxide production, which contributes to loss of Ca2+ homeostasis, and that induction of antioxidant defense systems is a mechanism underlying the [Ca2+]i‐stabilizing and excitoprotective actions of neurotrophic factors.
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Alzheimer's Ps-1 mutation perturbs calcium homeostasis and sensitizes Pc12 cells to death induced by amyloid β-peptide
Qing Guo,Katsutoshi Furukawa,Bryce L. Sopher,Dao G. Pham,Jun Xie,Nic Robinson,George M. Martin,Mark P. Mattson +7 more
TL;DR: It is reported that expression of PS-1 mutation L286V in cultured PC12 cells exaggerates Ca2+ responses to agonists (carbachol and bradykinin), and an antagonist of voltage-dependent calcium channels (nifedipine), and a blocker of Ca2- release from ER (dantrolene), counteract the adverse consequences of the PS- 1 mutation.
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18F-THK5351: A Novel PET Radiotracer for Imaging Neurofibrillary Pathology in Alzheimer Disease.
Ryuichi Harada,Nobuyuki Okamura,Shozo Furumoto,Katsutoshi Furukawa,Aiko Ishiki,Naoki Tomita,Tetsuro Tago,Kotaro Hiraoka,Shoichi Watanuki,Miho Shidahara,Masayasu Miyake,Yoichi Ishikawa,Rin Matsuda,Akie Inami,Takeo Yoshikawa,Yoshihito Funaki,Ren Iwata,Manabu Tashiro,Kazuhiko Yanai,Hiroyuki Arai,Yukitsuka Kudo +20 more
TL;DR: A novel tau PET tracer is developed through compound optimization of arylquinoline derivatives that bound to neurofibrillary tangles selectively and with a higher signal-to-background ratio than did THK5117 in Alzheimer disease patients.