Yasumasa Ohyagi

ORCID: 0000-0001-5720-3368
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About
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Research Areas
  • Alzheimer's disease research and treatments
  • Genetic Neurodegenerative Diseases
  • Multiple Sclerosis Research Studies
  • Amyotrophic Lateral Sclerosis Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Cholinesterase and Neurodegenerative Diseases
  • Mitochondrial Function and Pathology
  • Neurological diseases and metabolism
  • Neurogenetic and Muscular Disorders Research
  • Peripheral Neuropathies and Disorders
  • Advanced Neuroimaging Techniques and Applications
  • Cardiovascular Health and Disease Prevention
  • Neurological disorders and treatments
  • Parkinson's Disease Mechanisms and Treatments
  • Neuroscience and Neuropharmacology Research
  • Botulinum Toxin and Related Neurological Disorders
  • Hereditary Neurological Disorders
  • Nutrition and Health in Aging
  • Cerebrovascular and Carotid Artery Diseases
  • Advanced MRI Techniques and Applications
  • Dementia and Cognitive Impairment Research
  • Body Composition Measurement Techniques
  • Prion Diseases and Protein Misfolding
  • Myasthenia Gravis and Thymoma
  • Autoimmune Neurological Disorders and Treatments

Ehime University
2010-2024

Ehime University Hospital
2017

Kyushu University
2007-2016

Kyoto University
2016

Tokyo Women's Medical University
2009

Kyoto Prefectural University of Medicine
2009

Nagasaki University
2006

Japan Clinical Cancer Research Organization
2006

Nishikyushu University
2004

National Kyushu Medical Center
2001

The amyloid beta-protein (Abeta) ending at 42 plays a pivotal role in Alzheimer's disease (AD). We have reported previously that intracellular Abeta42 is associated with neuronal apoptosis vitro and vivo. Here, we show directly activated the p53 promoter, resulting p53-dependent apoptosis, Abeta40 had similar but lesser effect. Moreover, oxidative DNA damage induced nuclear localization of mRNA elevation guinea-pig primary neurons. Also, expression was elevated brain sporadic AD transgenic...

10.1096/fj.04-2637fje article EN The FASEB Journal 2004-11-17

Intracellular amyloid β-protein (Aβ) contributes to neurodegeneration in Alzheimer disease (AD). Apomorphine (APO) is a dopamine receptor agonist for Parkinson and also protects against oxidative stress. Efficacy of APO an AD mouse model effects on cell cultures are studied.The triple transgenic (3xTg-AD) has 2 familial AD-related gene mutations (APP(KM670/671NL) /PS1(M146V)) tau mutation (Tau(P301L)). Six-month-old 3xTg-AD mice were treated with subcutaneous injections once week 1 month....

10.1002/ana.22319 article EN Annals of Neurology 2010-10-29

In Alzheimer's disease (AD), the accumulation and deposition of amyloid-β (Aβ) peptides in brain is a central event. Aβ cleaved from amyloid precursor protein (APP) by β-secretase γ-secretase mainly neurons. Although mutations inAPP,PS1, orPS2cause early-onset familial AD,ABCA7encoding ATP-binding cassette transporter A7 one susceptibility genes for late-onset AD (LOAD), which itsloss-of-functionvariants increase risk. ABCA7 homologous to major lipid ABCA1 highly expressed neurons microglia...

10.1523/jneurosci.3757-15.2016 article EN cc-by-nc-sa Journal of Neuroscience 2016-03-30

Objective The objective of this study was to identify new causes Charcot–Marie–Tooth (CMT) disease in patients with autosomal‐recessive (AR) CMT. Methods To efficiently novel causative genes for AR‐CMT, we analyzed 303 unrelated Japanese CMT using whole‐exome sequencing and extracted recessive variants/genes shared among multiple patients. We performed mutation screening the newly identified membrane metalloendopeptidase ( MME ) gene 354 additional clinically, genetically, pathologically,...

10.1002/ana.24612 article EN cc-by-nc Annals of Neurology 2016-03-17

We have previously mapped autosomal dominant spinocerebellar ataxia (SCA) 16 to 3p26, overlapping with the locus of SCA15. Recently, partial deletions ITPR1 and neighbouring SUMF1 in SCA15 two additional families were reported. In present study we determined copy number these genes by real time quantitative polymerase chain reaction (PCR) found a heterozygous deletion exons 1-48 ITPR1, but not SCA16. Breakpoint analysis revealed that size is 313,318 bp telomeric breakpoint located middle...

10.1136/jmg.2007.053942 article EN Journal of Medical Genetics 2007-10-12

<b>BACKGROUND AND PURPOSE:</b> Cerebral hemodynamics abnormality in Alzheimer disease (AD) is not fully understood. Our aim was to determine whether regional hypoperfusion due AD associated with abnormalities arterial blood volume (rABV) and transit time (rATT) as measured by quantitative spin-labeling (ASL) multiple-delay sampling. <b>MATERIALS METHODS:</b> Nineteen patients (9 men 10 women; mean age, 74.5 ± 8.6 years) 22 cognitively healthy control subjects (11 11 72.8 6.8 were studied...

10.3174/ajnr.a1562 article EN cc-by American Journal of Neuroradiology 2009-04-02

Significance To extract critical information from Alzheimer’s disease (AD) postmortem brains that may otherwise be lost, we chose to screen epigenetic signatures. Epigenome analysis is a robust methodology in terms of its cell type and gene specificity, suitability for high-throughput analysis, resistance degradation. Analysis the neuron-specific methylome revealed variety differentially methylated genes, including BRCA1 . We demonstrate pathogenic relevance compromised genomic integrity by...

10.1073/pnas.1707151114 article EN public-domain Proceedings of the National Academy of Sciences 2017-10-17

<b><i>Objective:</i></b> To characterize a distinct form of autosomal dominant cerebellar ataxia (ADCA) clinically and genetically. <b><i>Background:</i></b> ADCAs are clinically, pathologically, genetically heterogeneous group neurodegenerative disorders. Nine responsible genes have been identified for SCA-1, -2, -3, -6, -7, -8, -10, -12 dentatorubral-pallidoluysian atrophy (DRPLA). Loci SCA-4, -5, -11, -13, -14 mapped. <b><i>Methods:</i></b> The authors studied four-generation Japanese...

10.1212/wnl.57.1.96 article EN Neurology 2001-07-10

To investigate cytokine/chemokine changes in amyotrophic lateral sclerosis (ALS), we simultaneously measured 16 cytokine/chemokines (interleukin [IL]-1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12 [p70], IL-13, IL-17, interferon-gamma, tumor necrosis factor-alpha, granulocyte colony stimulating factor [G-CSF], macrophage chemoattractant protein-1 [MCP-1], and inflammatory protein-1beta) cerebrospinal fluid (CSF) sera from 37 patients with sporadic ALS 33 controls using a multiplexed...

10.1097/01.jnen.0000232025.84238.e1 article EN Journal of Neuropathology & Experimental Neurology 2006-08-01

Abstract Fibrodysplasia ossificans progressiva (FOP) is a rare autosomal dominant congenital disease characterized by progressive heterotopic endochondral osteogenesis with great‐toe malformations. A 617G &gt; (R206H) mutation of the activin type 1 receptor gene ( ACVR1 ) has been found in all previously reported patients FOP. Thus, this one most specific disease‐associated mutations. We report here on 62‐year‐old man slowly FOP and novel . He developed difficulty moving his shoulder since...

10.1002/ajmg.a.32151 article EN American Journal of Medical Genetics Part A 2008-01-17

There are two distinct subtypes of multiple sclerosis (MS) in Asians: opticospinal (OSMS) and conventional (CMS). OSMS has similar features to neuromyelitis optica (NMO) half patients have the NMO-Immunoglobulin G (IgG)/ anti-aquaporin-4 (AQP4) antibody. We reported that Helicobacter pylori (H. pylori) infection was significantly less common CMS than controls. To reveal immune responses H. neutrophil-activating protein (HP-NAP) Japanese MS patients, according anti-AQP4 antibody status, sera...

10.1177/1352458509348961 article EN Multiple Sclerosis Journal 2009-11-13

Amyloid-β protein (Aβ) accumulates in the neurons of Alzheimer's disease (AD) patients at an early stage disease. Recently, we found that Aβ with a toxic turn positions 22 and 23 AD brain. Here, studied accumulation Aβ, high-molecular-weight oligomers presenilin 1 (PS1) gene-transfected SH-SY5Y cells as well brains 3xTg-AD mice patients. Immunostaining revealed was promoted G384A- I143T-mutant PS1-transfected further enhanced by co-transfection Aβ-precursor (AβPP) gene. In contrast, mutant...

10.2174/156720513804871372 article EN Current Alzheimer Research 2013-01-01

The toxic conformer of amyloid β-protein (Aβ) ending at 42 (Aβ42), which contains a unique turn conformation amino acid residue positions 22 and 23 tends to form oligomers that are neurotoxic, was reported play critical role in the pathomechanisms Alzheimer's disease (AD), diabetes mellitus (DM)-like mechanisms also suggested be operative. It remains established whether attenuation insulin signaling is involved an increase Aβ42 levels. present study investigated association between impaired...

10.1016/j.nbd.2020.104739 article EN cc-by Neurobiology of Disease 2020-01-10

We investigated the mechanisms underlying abnormal vascular endothelial growth factor (VEGF) production in amyotrophic lateral sclerosis (ALS). immunohistochemically studied VEGF, its receptors VEGFR1 and 2, hypoxia-inducible factor-1α (HIF-1α) autopsied ALS spinal cords. also chronologically assessed expression of HIF-1α, karyopherin β1, β-cargo protein complex inhibitors nuclear pore proteins G93A mutant superoxide dismutase 1 (mSOD1) transgenic mice at presymptomatic, symptomatic end...

10.1111/bpa.12040 article EN Brain Pathology 2013-01-31

One-leg standing time (OLST) has been frequently used physical performance measure; however, what muscular characteristics OLST represents remains uncertain. This cross-sectional study aimed to investigate the association between and muscle clarify possibility of using as a measure. Study participants comprised 1144 older adults aged 65 years or older. Computed tomography images provided mid-thigh skeletal area mean attenuation value. was measured for maximum 60 s. Static postural...

10.1007/s40520-023-02665-8 article EN cc-by Aging Clinical and Experimental Research 2024-01-28
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