Masato Kanazawa

ORCID: 0000-0001-6337-8156
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About
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Research Areas
  • Parkinson's Disease Mechanisms and Treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Acute Ischemic Stroke Management
  • Genetic Neurodegenerative Diseases
  • Neurological Disease Mechanisms and Treatments
  • Mitochondrial Function and Pathology
  • Neurological disorders and treatments
  • Angiogenesis and VEGF in Cancer
  • Mesenchymal stem cell research
  • Amyotrophic Lateral Sclerosis Research
  • Cerebrovascular and genetic disorders
  • Alzheimer's disease research and treatments
  • Metabolism and Genetic Disorders
  • Neurological and metabolic disorders
  • Ophthalmology and Eye Disorders
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Neurological Disorders and Treatments
  • Neurogenesis and neuroplasticity mechanisms
  • Moyamoya disease diagnosis and treatment
  • Protease and Inhibitor Mechanisms
  • Neurological Complications and Syndromes
  • Intracranial Aneurysms: Treatment and Complications
  • Diabetes Management and Research
  • Cardiovascular Syncope and Autonomic Disorders
  • Autoimmune Neurological Disorders and Treatments

Niigata University
2016-2025

University of Washington
2011-2017

Okayama University
2015

SAGA Heavy Ion Medical Accelerator in Tosu
2013-2015

Shibaura Institute of Technology
2011

Chiba Kaihin Municipal Hospital
1997-2008

Fukushima Medical University
2007

Fukuoka University
2007

Sado General Hospital
2006-2007

Research Institute for Brain and Blood Vessels Akita
2007

The hypothesis tested by these studies states that in addition to interendothelial cell tight junction proteins, matrix adhesion β 1 -integrin receptors expressed endothelial cells have an important role maintaining the cerebral microvessel permeability barrier. Primary brain from C57 BL/6 mice were incubated with -rintegrin function-blocking antibody (Ha2/5) or isotype control and impacts on claudin-5 expression quantified. Both flow cytometry immunofluorescence demonstrated confluent was...

10.1038/jcbfm.2011.99 article EN Journal of Cerebral Blood Flow & Metabolism 2011-07-20

Hemorrhage and edema accompany evolving brain tissue injury after ischemic stroke. In patients, these events have been associated with metalloproteinase (MMP)-9 in plasma. Both the causes cellular sources of MMP-9 generation this setting not defined. MMP-2 nonhuman primate regions plasma leakage, primary murine microglia astrocytes, were assayed by immunocytochemistry, zymography, real-time RT-PCR. Ischemia-related hemorrhage was microglial activation vivo, leakage fibronectin vitronectin...

10.1038/jcbfm.2012.11 article EN Journal of Cerebral Blood Flow & Metabolism 2012-02-22

In the central nervous system, progranulin, a glycoprotein growth factor, plays crucial role in maintaining physiological functions, and progranulin gene mutations cause TAR DNA-binding protein-43-positive frontotemporal lobar degeneration. Although several studies have reported that protective against ischaemic brain injury, little is known about temporal changes expression level, cellular localization, glycosylation status of after acute focal cerebral ischaemia. addition, precise...

10.1093/brain/awv079 article EN Brain 2015-04-02

The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson's syndrome (RS) and PSP-Parkinsonism (PSP-P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. investigated features both early in at any time during disease course. pathological severities neuronal loss gliosis tau pathology were also evaluated. On basis...

10.1002/mds.22583 article EN Movement Disorders 2009-05-01

Abstract Cell-therapies that invoke pleiotropic mechanisms may facilitate functional recovery in stroke patients. We hypothesized a cell therapy using microglia preconditioned by optimal oxygen-glucose deprivation (OGD) is therapeutic strategy for ischemic because ischemia induces anti-inflammatory M2 microglia. first delineated changes angiogenesis and axonal outgrowth the cortex rats. found slight without were activated at border area within core from 7 to 14 days after ischemia. Next, we...

10.1038/srep42582 article EN cc-by Scientific Reports 2017-02-14

An angiogenic factor, vascular endothelial growth factor (VEGF), might be associated with the blood-brain barrier (BBB) disruption after focal cerebral ischemia; however, it remains unknown whether hemorrhagic transformation (HT) tissue plasminogen activator (tPA) treatment is related to activation of VEGF signaling pathway in BBB. Here, we hypothesized that inhibition can attenuate HT tPA treatment. Rats subjected thromboembolic ischemia were assigned a permanent group and groups treated at...

10.1038/jcbfm.2011.9 article EN cc-by Journal of Cerebral Blood Flow & Metabolism 2011-02-09

Acutely following focal cerebral ischemia disruption of the microvessel blood-brain barrier allows transit plasma proteins into neuropil as edema formation that coincides with loss endothelial β1-integrins. We extend previous findings to show interference β1-integrin-matrix adhesion by monoclonal IgM Ha2/5 increases permeability primary microvascular cell monolayers through reorganization claudin-5, occludin, and zonula occludens-1 (ZO-1) from inter-endothelial borders. Interference...

10.1177/0271678x17722108 article EN Journal of Cerebral Blood Flow & Metabolism 2017-08-08

Clinical manifestations of methylmercury (MeHg) intoxication include cerebellar ataxia, concentric constriction visual fields, and sensory auditory disturbances. The symptoms depend on the site MeHg damage, such as cerebellum occipital lobes. However, underlying mechanism MeHg-induced tissue vulnerability remains to be elucidated. In present study, we used a rat model subacute investigate possible blood-brain barrier (BBB) damage. was established by exposing rats 20-ppm for up 4 weeks;...

10.1371/journal.pone.0170623 article EN cc-by PLoS ONE 2017-01-24

Cryptococcal meningoencephalitis (CM) in human immunodeficiency virus (HIV)-negative patients are often diagnosed later than HIV-infected patients, which increases mortality rates concerning the former. Consequently, early diagnosis and treatment crucial for improving clinical prognosis HIV-negative patients. This study investigated utility of magnetic resonance imaging (MRI) combination with laboratory findings CM retrospective cohort analysis included consecutive central nervous system...

10.1016/j.ensci.2025.100552 article EN cc-by-nc-nd eNeurologicalSci 2025-01-09

We investigated the incidence and clinical features of patients with myasthenia gravis (MG) associated autoimmune diseases. Associated diseases were found in 28 142 consecutive Japanese MG (19.7%), amongst which Graves’ disease (7.7%) Hashimoto's thyroiditis (4.2%) predominant. The different from those without terms age at onset symptoms (35.5 ± 4.0 years 49.0 1.7 years; P < 0.05), positivity for anti‐acetylcholine receptor antibody (44.4% 89.8%; association thymic hyperplasia (72.7...

10.1111/j.1468-1331.2007.01978.x article EN European Journal of Neurology 2007-10-18

Abstract The clinical presentation of corticobasal degeneration is diverse, while the background pathology syndrome also heterogeneous. Therefore, predicting pathological extremely difficult. Herein, we investigated findings and course in patients with pathologically, genetically biochemically verified to determine suggestive disorder. Thirty-two were identified as having degeneration. median intervals from initial symptoms onset key milestones follows: gait disturbance, 0.0 year;...

10.1093/braincomms/fcad296 article EN cc-by Brain Communications 2023-01-01

The role of HSDJ, a human homolog bacterial DnaJ and yeast YDJ1p/MAS5, in mitochondrial protein import was examined. Recombinant HSDJ purified an antibody prepared. mRNA heat-induced cultured cells. In pulse-labeling chase experiments using COS-7 cells, the endogenous prenylated. Transiently expressed also prenylated, whereas its mutant C394S which cysteine "CaaX box" mutated to serine, not. but not C394S, synthesized rabbit reticulocyte lysate farnesylated. inhibited ornithine...

10.1093/oxfordjournals.jbchem.a021670 article EN The Journal of Biochemistry 1997-05-01

<b><i><i>Objective:</i></i></b> To assess alterations in brain metabolites patients with late-onset ornithine transcarbamylase deficiency (OTCD). <b><i><i>Methods:</i></i></b> Six unrelated, asymptomatic Japanese OTCD were analyzed by proton MRS (<sup>1</sup>HMRS) using a point-resolved spectroscopy technique (repetition and echo times, 5000 30 ms). Localized spectra for the centrum semiovale acquired absolute metabolite concentrations calculated an LCModel. <b><i><i>Results:</i></i></b>...

10.1212/wnl.59.2.210 article EN Neurology 2002-07-23

Nuclear factor TAR DNA-binding protein-43 (TDP-43) is considered to play roles in pathogenesis of human neurodegenerative diseases, so-called TDP-43 proteinopathy, via its proteolytic cleavage, abnormal phosphorylation, subcellular redistribution, and insolubilization generating TDP-43-positive neuronal intracellular inclusions. The purpose this study was elucidate biochemical histopathological alternations specific acute ischemic stroke. Adult male rats were subjected a 90-min middle...

10.1111/j.1471-4159.2010.06860.x article EN Journal of Neurochemistry 2010-06-14
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