Zobrazeno 1 - 10
of 29
pro vyhledávání: '"Naoto Watamura"'
Autor:
Shoko Hashimoto, Yukio Matsuba, Mika Takahashi, Naoko Kamano, Naoto Watamura, Hiroki Sasaguri, Yuhei Takado, Yoshihiro Yoshihara, Takashi Saito, Takaomi C. Saido
Publikováno v:
Scientific Reports, Vol 13, Iss 1, Pp 1-18 (2023)
Abstract Accumulating evidence suggests that glutathione loss is closely associated with the progression of neurodegenerative disorders. Here, we found that the neuronal conditional-knockout (KO) of glutamyl-cysteine-ligase catalytic-subunit (GCLC),
Externí odkaz:
https://doaj.org/article/0e2d8155c464445c84a3c0e68311ab35
Autor:
Richeng Jiang, Una Smailovic, Hazal Haytural, Betty M. Tijms, Hao Li, Robert Mihai Haret, Ganna Shevchenko, Gefei Chen, Axel Abelein, Johan Gobom, Susanne Frykman, Misaki Sekiguchi, Ryo Fujioka, Naoto Watamura, Hiroki Sasaguri, Sofie Nyström, Per Hammarström, Takaomi C. Saido, Vesna Jelic, Stina Syvänen, Henrik Zetterberg, Bengt Winblad, Jonas Bergquist, Pieter Jelle Visser, Per Nilsson
Publikováno v:
Acta Neuropathologica Communications, Vol 10, Iss 1, Pp 1-17 (2022)
Abstract Cerebrospinal fluid (CSF) biomarkers play an important role in diagnosing Alzheimer’s disease (AD) which is characterized by amyloid-β (Aβ) amyloidosis. Here, we used two App knock-in mouse models, App NL-F/NL-F and App NL-G-F/NL-G-F , e
Externí odkaz:
https://doaj.org/article/de02c2b3c0b44a69941ed429ae504a9a
Autor:
Hiroki Sasaguri, Shoko Hashimoto, Naoto Watamura, Kaori Sato, Risa Takamura, Kenichi Nagata, Satoshi Tsubuki, Toshio Ohshima, Atsushi Yoshiki, Kenya Sato, Wakako Kumita, Erika Sasaki, Shinobu Kitazume, Per Nilsson, Bengt Winblad, Takashi Saito, Nobuhisa Iwata, Takaomi C. Saido
Publikováno v:
Frontiers in Neuroscience, Vol 16 (2022)
Since 1995, more than 100 transgenic (Tg) mouse models of Alzheimer’s disease (AD) have been generated in which mutant amyloid precursor protein (APP) or APP/presenilin 1 (PS1) cDNA is overexpressed (1st generation models). Although many of these m
Externí odkaz:
https://doaj.org/article/3983cddf12fe4239a47976b7e939da42
Autor:
Nobuhisa Iwata, Satoshi Tsubuki, Misaki Sekiguchi, Kaori Watanabe-Iwata, Yukio Matsuba, Naoko Kamano, Ryo Fujioka, Risa Takamura, Naoto Watamura, Naomasa Kakiya, Naomi Mihira, Takahiro Morito, Keiro Shirotani, Mann, David M. A., Robinson, Andrew C., Shoko Hashimoto, Hiroki Sasaguri, Takashi Saito, Makoto Higuchi, Saido, Takaomi C.
Publikováno v:
Life Science Alliance; Dec2024, Vol. 7 Issue 12, p1-17, 17p
Autor:
Hiroki Sasaguri, Takaomi C. Saido, Naoto Watamura, Naoko Kamano, Satoshi Tsubuki, Shoko Hashimoto, Per Nilsson, Takashi Saito, Naomasa Kakiya, Mika Takahashi
Publikováno v:
Molecular Psychiatry. 27:1816-1828
Alzheimer’s disease (AD) is characterized by the deposition of amyloid β peptide (Aβ) in the brain. The neuropeptide somatostatin (SST) regulates Aβ catabolism by enhancing neprilysin (NEP)-catalyzed proteolytic degradation. However, the mechani
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::1e001216b077bc97f0865e8d2cb321f6
https://doi.org/10.1038/s41380-021-01368-8
https://doi.org/10.1038/s41380-021-01368-8
Autor:
Naoto Watamura, Kaori Sato, Gen Shiihashi, Ayami Iwasaki, Naoko Kamano, Mika Takahashi, Misaki Sekiguchi, Naomi Mihira, Ryo Fujioka, Kenichi Nagata, Shoko Hashimoto, Takashi Saito, Toshio Ohshima, Takaomi C. Saido, Hiroki Sasaguri
Publikováno v:
Science Advances. 8
We previously developed single App knock-in mouse models of Alzheimer’s disease (AD) that harbor the Swedish and Beyreuther/Iberian mutations with or without the Arctic mutation ( App NL-G-F and App NL-F mice). We have now generated App knock-in mi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::07fa8043c2e80015ca1734038a06394a
https://doi.org/10.1126/sciadv.abm6155
https://doi.org/10.1126/sciadv.abm6155
Autor:
Hiroki Sasaguri, Shoko Hashimoto, Naoto Watamura, Kaori Sato, Risa Takamura, Kenichi Nagata, Satoshi Tsubuki, Toshio Ohshima, Atsushi Yoshiki, Kenya Sato, Wakako Kumita, Erika Sasaki, Shinobu Kitazume, Per Nilsson, Bengt Winblad, Takashi Saito, Nobuhisa Iwata, Takaomi C. Saido
Publikováno v:
Frontiers in neuroscience. 16
Since 1995, more than 100 transgenic (Tg) mouse models of Alzheimer’s disease (AD) have been generated in which mutant amyloid precursor protein (APP) or APP/presenilin 1 (PS1) cDNA is overexpressed (1st generation models). Although many of these m
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f6d3ffabc5aa47defe0e0f36ca449dad
https://pubmed.ncbi.nlm.nih.gov/35431779
https://pubmed.ncbi.nlm.nih.gov/35431779
Publikováno v:
Neurochemistry International. 158:105361
Most mouse models for preclinical research into Alzheimer's disease (AD) rely on the overexpression paradigm, in which familial AD (FAD)-related genes linked to amyloid precursor protein (APP) and presenilin-1 (PSEN1) are overexpressed. Such mice hav
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::846da754ecb7e353257d473189475fa8
https://doi.org/10.1016/j.neuint.2022.105361
https://doi.org/10.1016/j.neuint.2022.105361
Autor:
Naomi Yamazaki, Toshio Ohshima, Shoko Hashimoto, Naomasa Kakiya, Ryo Fujioka, Takaomi C. Saido, Naoto Watamura, Kaori Iwata, Satoshi Tsubuki, Yukio Matsuba, Nobuhisa Iwata, Takashi Saito, Risa Takamura, Hiroki Sasaguri, Misaki Sekiguchi
Neprilysin (NEP) and insulin-degrading enzyme (IDE) are considered the two major catabolic enzymes that degrade amyloid β peptide (Aβ), the primary cause of Alzheimer’s disease (AD). However, their roles in Aβ metabolism in vivo have never been
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::5f7436d03f7d6322e40d4cdade11f492
https://doi.org/10.1101/2021.08.22.457281
https://doi.org/10.1101/2021.08.22.457281
Autor:
Naoko Kamano, Takashi Saito, Gen Shiihashi, Naomi Yamazaki, Ayami Iwasaki, Mika Takahashi, Shoko Hashimoto, Ryo Fujioka, Toshio Ohshima, Kenichi Nagata, Misaki Sekiguchi, Takaomi C. Saido, Hiroki Sasaguri, Kaori Sato, Naoto Watamura
SUMMARYWe previously developed single App knock-in mouse models of Alzheimer’s disease (AD) that harbor the Swedish and Beyreuther/Iberian mutations with or without the Arctic mutation (AppNL- G-F and AppNL-F mice). These models showed the developm
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::f43e26f67c71a03140aaf1edbf7d18c0
https://doi.org/10.1101/2021.08.22.457278
https://doi.org/10.1101/2021.08.22.457278