Zobrazeno 1 - 10
of 218
pro vyhledávání: '"Makoto, Michikawa"'
Autor:
Tomohisa Nakamura, Tadahiro Hashita, Yuxin Chen, Yuan Gao, Yang Sun, Sadequl Islam, Hiroyuki Sato, Yasuyuki Shibuya, Kun Zou, Tamihide Matsunaga, Makoto Michikawa
Publikováno v:
Molecular Brain, Vol 16, Iss 1, Pp 1-10 (2023)
Abstract Our previous study showed that the flotillin level is decreased in the blood of patients with Alzheimer’s disease (AD) when compared to that of patients with non-AD and vascular dementia; however, the molecular mechanism remains to be dete
Externí odkaz:
https://doaj.org/article/05c0118f6d794355858bce286552e92e
Autor:
Abu Zaffar Shibly, Abdullah Md. Sheikh, Makoto Michikawa, Shatera Tabassum, Abul Kalam Azad, Xiaojing Zhou, Yuchi Zhang, Shozo Yano, Atsushi Nagai
Publikováno v:
Biomedicines, Vol 12, Iss 1, p 104 (2024)
In the original publication [...]
Externí odkaz:
https://doaj.org/article/2865f76395964b1cb4b1d112e0d6a194
Autor:
Cha-Gyun Jung, Reiko Kato, Chunyu Zhou, Mona Abdelhamid, Esraa Ibrahim A. Shaaban, Hitoshi Yamashita, Makoto Michikawa
Publikováno v:
Scientific Reports, Vol 12, Iss 1, Pp 1-11 (2022)
Abstract Global warming is a serious public health threat to people worldwide. High body temperature is one of the important risk factors for Alzheimer’s disease (AD), and the body temperature of AD patients has been found to be significantly highe
Externí odkaz:
https://doaj.org/article/f330424fb06a4a9792d424388bbf731a
Autor:
Yuan Gao, Yang Sun, Sadequl Islam, Tomohisa Nakamura, Taisuke Tomita, Kun Zou, Makoto Michikawa
Publikováno v:
Frontiers in Aging Neuroscience, Vol 15 (2023)
IntroductionAlzheimer’s disease (AD) is associated with amyloid β-protein 1-42 (Aβ42) accumulation in the brain. Aβ42 and Aβ40 are the major two species generated from amyloid precursor protein. We found that angiotensin-converting enzyme (ACE)
Externí odkaz:
https://doaj.org/article/1cb3d4484e2f4f52ae2a4c15b051d2d1
Autor:
Kun Zou, Sadequl Islam, Yang Sun, Yuan Gao, Tomohisa Nakamura, Hiroto Komano, Taisuke Tomita, Makoto Michikawa
Publikováno v:
Frontiers in Aging Neuroscience, Vol 14 (2022)
Alzheimer’s disease (AD) is a genetic and sporadic neurodegenerative disease characterized by extracellular amyloid-β-protein (Aβ) aggregates as amyloid plaques and neuronal loss in the brain parenchyma of patients. Familial AD (FAD) is found to
Externí odkaz:
https://doaj.org/article/b1ed4283d0c34a38b03026aceee3a6b5
Autor:
Mohammad Abdullah, Tomohisa Nakamura, Taslima Ferdous, Yuan Gao, Yuxin Chen, Kun Zou, Makoto Michikawa
Publikováno v:
Frontiers in Immunology, Vol 12 (2021)
Exosomes are vesicles secreted by various kinds of cells, and they are rich in cholesterol, sphingomyelin (SM), phosphatidylcholine, and phosphatidylserine. Although cellular sphingolipid-mediated exosome release has been reported, the involvement of
Externí odkaz:
https://doaj.org/article/5c8f9452871d4e7e949b7c9b1a876e9b
Autor:
Abu Zaffar Shibly, Abdullah Md. Sheikh, Makoto Michikawa, Shatera Tabassum, Abul Kalam Azad, Xiaojing Zhou, Yuchi Zhang, Shozo Yano, Atsushi Nagai
Publikováno v:
Biomedicines, Vol 11, Iss 1, p 50 (2022)
Amyloid β (Aβ) peptide is deposited in the brains of sporadic Alzheimer’s disease (AD) due to impaired vessel-dependent clearance. To understand the mechanisms, we investigated time-dependent cerebrovascular changes in AD model mice. Cerebrovascu
Externí odkaz:
https://doaj.org/article/2f30aa809c574cd29fd9703b5a6e4f66
Autor:
Keiko Honda, Yuhki Saito, Haruka Saito, Megumi Toyoda, Ruriko Abe, Takashi Saito, Takaomi C. Saido, Makoto Michikawa, Hidenori Taru, Yuriko Sobu, Saori Hata, Tadashi Nakaya, Toshiharu Suzuki
Publikováno v:
Neurobiology of Aging. 123:63-74
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::874979664c20ded1c9009ca31d15167f
https://doi.org/10.1016/j.neurobiolaging.2022.12.003
https://doi.org/10.1016/j.neurobiolaging.2022.12.003
Publikováno v:
Journal of Neurochemistry. 164:858-874
The mechanisms of amyloid accumulation in familial Alzheimer's disease (FAD) and sporadic AD (SAD) are controversial. In FAD, mutations in presenilin (PSEN) impair γ-secretase activity and lead to abnormal amyloid β-protein (Aβ) production, thereb
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7a9bbf6cc758cb23c6b5989dc9d45587
https://doi.org/10.1111/jnc.15750
https://doi.org/10.1111/jnc.15750
Autor:
TETSURO MORIKAWA, OSAMU UEHARA, DURGA PAUDEL, KOKI YOSHIDA, FUMIYA HARADA, DAICHI HIRAKI, JUN SATO, HIROFUMI MATSUOKA, YASUHIRO KURAMITSU, MAKOTO MICHIKAWA, YOSHIHIRO ABIKO
Publikováno v:
In Vivo. 37:163-172
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::1f563cdac917c26b20d96c9a8f2b36cb
https://doi.org/10.21873/invivo.13065
https://doi.org/10.21873/invivo.13065