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Genomes and Genes | Yoko OkamotoSummaryAffiliation: Kyoto University Country: Japan Publications
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Publications
Cortical microinfarcts in Alzheimer's disease and subcortical vascular dementiaYoko Okamoto
Department of Neurology, Graduate School of Medicine, Kyoto University, Kyoto, Japan
Neuroreport 20:990-6. 2009..These results indicate that cortical microinfarcts are caused by the pathomechanism related to Alzheimer's disease, most likely to amyloid angiopathy...- Synthesis and biological evaluation of novel styryl benzimidazole derivatives as probes for imaging of neurofibrillary tangles in Alzheimer's diseaseKenji Matsumura
Department of Patho Functional Bioanalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, 46 29 Yoshida Shimoadachi cho, Sakyo ku, Kyoto 606 8501, Japan
Bioorg Med Chem 21:3356-62. 2013..12-0.33%ID/g at 60min after the injection) the brain. In conclusion, appropriate structural modifications of SBIM derivatives could lead to more useful agents for the in vivo imaging of NFT in AD brains... - Selective white matter abnormalities in a novel rat model of vascular dementiaAkihiro Kitamura
Department of Neurology, Graduate School of Medicine, Kyoto University, Sakyo ku, Kyoto, Japan
Neurobiol Aging 33:1012.e25-35. 2012..This led to significant spatial working memory impairment of a magnitude similar to the 2VO rats at 28 days postoperation. The 2VGO model may more closely mimic cognitive impairment subsequent to selective white matter damage... 
Cerebral hypoperfusion accelerates cerebral amyloid angiopathy and promotes cortical microinfarctsYoko Okamoto
Department of Neurology, Kyoto University Graduate School of Medicine, 54 Kawaharacho, Shogoin, Sakyo, Kyoto 606 8507, Japan
Acta Neuropathol 123:381-94. 2012..Our results suggest that cerebral hypoperfusion accelerates CAA, and thus promotes CMIs...- Cilostazol, a phosphodiesterase inhibitor, prevents no-reflow and hemorrhage in mice with focal cerebral ischemiaYoshiki Hase
Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan
Exp Neurol 233:523-33. 2012..Particular emphasis will be placed on the plasma-microvessel interface... - Rhodanine and thiohydantoin derivatives for detecting tau pathology in Alzheimer's brainsMasahiro Ono
Graduate School of Pharmaceutical Sciences, Kyoto University, 46 29 Yoshida Shimoadachi cho, Sakyo ku, Kyoto 606 8501, Japan
ACS Chem Neurosci 2:269-75. 2011..54%ID/g, 2 min postinjection) into and a rapid washout (0.25%ID/g, 60 min postinjection) from the brain. [(123)I]TH2 should be further investigated as a potential imaging agent for detecting tau pathology... - Novel ¹⁸F-labeled benzoxazole derivatives as potential positron emission tomography probes for imaging of cerebral β-amyloid plaques in Alzheimer's diseaseMengchao Cui
Department of Patho Functional Bioanalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, 46 29 Yoshida Shimoadachi cho, Sakyo ku, Kyoto 606 8501, Japan
J Med Chem 55:9136-45. 2012..The results suggest [(18)F]24 to be a useful PET agent for detecting Aβ plaques in the living human brain... - Synthesis and biological evaluation of novel oxindole derivatives for imaging neurofibrillary tangles in Alzheimer's diseaseHiroyuki Watanabe
Department of Patho Functional Bioanalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, 46 29 Yoshida Shimoadachi cho, Sakyo ku, Kyoto 606 8501, Japan
Bioorg Med Chem Lett 22:5700-3. 2012..6-1.4%ID/g at 30 min). In fluorescence staining experiments using AD brain sections, 14 clearly stained NFTs. 3-OI may serve as a new molecular scaffold for developing novel NFT imaging agents... - Clinicopathologic study on an ALS family with a heterozygous E478G optineurin mutationHidefumi Ito
Department of Neurology, Kyoto University Graduate School of Medicine, Shogoin, Sakyo ku, Japan
Acta Neuropathol 122:223-9. 2011..We postulate that optineurinopathy is closely linked with TDP-proteinopathy and speculate that this heterozygous E478G mutation would cause ALS by acting through a dominant-negative mechanism... - The influence of chronic cerebral hypoperfusion on cognitive function and amyloid β metabolism in APP overexpressing miceMahito Yamada
Department of Neurology, Graduate School of Medicine, Kyoto University, Kyoto, Japan
PLoS ONE 6:e16567. 2011..Therefore, we investigated whether chronic cerebral hypoperfusion influences cognitive ability or amyloid β deposition in amyloid precursor protein (APP) overexpressing transgenic mice... 
Leukoencephalopathy with cognitive impairment following tocilizumab for the treatment of rheumatoid arthritis (RA)Katsuya Kobayashi
Department of Neurology, Kyoto University Hospital, Kyoto
Intern Med 48:1307-9. 2009..The leukoencephalopathy might have been caused by a mechanism related to tocilizumab itself. It is strongly recommended to perform MRI if a patient develops any cognitive impairment during tocilizumab therapy...- Colocalization of 14-3-3 proteins with SOD1 in Lewy body-like hyaline inclusions in familial amyotrophic lateral sclerosis cases and the animal modelYoko Okamoto
Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan
PLoS ONE 6:e20427. 2011..To further investigate the role of 14-3-3 proteins in ALS, we performed immunohistochemical analysis of 14-3-3 proteins and compared their distributions with those of SOD1 in FALS patients and SOD1-overexpressing mice...