Zobrazeno 1 - 10
of 141
pro vyhledávání: '"Masuo Ohno"'
Autor:
Masuo Ohno
Publikováno v:
Neuropsychopharmacology Reports, Vol 41, Iss 2, Pp 255-259 (2021)
Abstract Aim After the continued failure of β‐secretase (BACE1) inhibitor clinical trials in prodromal as well as mild‐to‐moderate Alzheimer's disease (AD), they are shifting to further earlier or asymptomatic stages. The aim of this study is
Externí odkaz:
https://doaj.org/article/ccdd54dd60794276a4a245e294c90d55
Autor:
Latha Devi, Masuo Ohno
Publikováno v:
Neurobiology of Disease, Vol 45, Iss 1, Pp 417-424 (2012)
Mitochondrial dysfunction is an early feature of Alzheimer's disease (AD) and may play an important role in the pathogenesis of disease. Emerging evidence indicates that amyloid-β (Aβ) peptides enter mitochondria and may thereby disrupt mitochondri
Externí odkaz:
https://doaj.org/article/4f5dd24e9ee24699bfbac71e7a0b1c12
Autor:
Ryoichi Kimura, Masuo Ohno
Publikováno v:
Neurobiology of Disease, Vol 33, Iss 2, Pp 229-235 (2009)
Although animal models of Alzheimer's disease (AD) recapitulate β-amyloid-dependent hippocampal synaptic and cognitive dysfunctions, it is poorly understood how cortex-dependent remote memory stabilization following initial hippocampal coding is aff
Externí odkaz:
https://doaj.org/article/83006d5ded0a4d8ea568c00c389968aa
Autor:
Masuo Ohno, Sarah L. Cole, Marina Yasvoina, Jie Zhao, Martin Citron, Robert Berry, John F. Disterhoft, Robert Vassar
Publikováno v:
Neurobiology of Disease, Vol 26, Iss 1, Pp 134-145 (2007)
Evidence suggests that β-amyloid (Aβ) peptide triggers a pathogenic cascade leading to neuronal loss in Alzheimer’s disease (AD). However, the causal link between Aβ and neuron death in vivo remains unclear since most animal models fail to recap
Externí odkaz:
https://doaj.org/article/4c60bc4225294b41a4c3251f0b971304
Autor:
Latha Devi, Masuo Ohno
Publikováno v:
PLoS ONE, Vol 8, Iss 10, p e77335 (2013)
Emerging evidence suggests that dysregulated translation through phosphorylation of eukaryotic initiation factor-2α (eIF2α) may contribute to Alzheimer's disease (AD) and related memory impairments. However, the underlying mechanisms remain unclear
Externí odkaz:
https://doaj.org/article/f503d945d7e04b5f8d68eead39a1516a
Publikováno v:
PLoS ONE, Vol 7, Iss 3, p e32792 (2012)
Although evidence is accumulating that diabetes mellitus is an important risk factor for sporadic Alzheimer's disease (AD), the mechanisms by which defects in insulin signaling may lead to the acceleration of AD progression remain unclear. In this st
Externí odkaz:
https://doaj.org/article/5e26c55cf8d74b1eaf2714969bcb1bbf
Autor:
Latha Devi, Masuo Ohno
Publikováno v:
PLoS ONE, Vol 5, Iss 9, p e12974 (2010)
β-Site APP-cleaving enzyme 1 (BACE1) initiates amyloid-β (Aβ) generation and thus represents a prime therapeutic target in treating Alzheimer's disease (AD). Notably, increasing evidence indicates that BACE1 levels become elevated in AD brains as
Externí odkaz:
https://doaj.org/article/838e313995d84c8b94a0557c16637353
Autor:
Masuo Ohno
Publikováno v:
Frontiers in Dementia. 2
Given a long preclinical stage of Alzheimer's disease (AD) continuum before the onset of dementia, there is a growing demand for tools capable of detecting the earliest feature of subtle cognitive impairment and optimizing recruitment to clinical tri
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::cf025e7001652fea8c9c752c5f107430
https://doi.org/10.3389/frdem.2023.1161875
https://doi.org/10.3389/frdem.2023.1161875
Autor:
Masuo Ohno
Publikováno v:
Brain Research Bulletin. 141:72-78
Cell signaling in response to an array of diverse stress stimuli converges on the phosphorylation of eukaryotic initiation factor-2α (eIF2α). In the brain, eIF2α is a hub for controlling learning and memory function and for maintaining neuronal in
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::61a85452a33a930e00413b713e3942d4
https://doi.org/10.1016/j.brainresbull.2017.08.007
https://doi.org/10.1016/j.brainresbull.2017.08.007
Autor:
Latha Devi, Masuo Ohno
Publikováno v:
Neuroscience. 307:128-137
β-Site APP-cleaving enzyme 1 (BACE1) initiates the generation of amyloid-β (Aβ), thus representing a prime therapeutic target for Alzheimer's disease (AD). Previous work including ours has used BACE1 haploinsufficiency (BACE1(+/-); i.e., 50% reduc
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::022ac679cdf6b3f894a50e213e855a0a
https://doi.org/10.1016/j.neuroscience.2015.08.037
https://doi.org/10.1016/j.neuroscience.2015.08.037