4 results match your criteria: "Yumoto Institute of Neurology[Affiliation]"
J Alzheimers Dis
August 2019
Department of Physics, College of Humanities and Sciences, Nihon University, Sakurajousui, Setagaya-ku, Tokyo, Japan.
Increasing evidence indicates that metal-induced oxidative stress plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). Recently, the presence of 8-hydroxydeoxyguanosine, a biomarker of oxidative DNA damage, was demonstrated in nuclear DNA (nDNA) in the AD brain. Iron (Fe) is a pro-oxidant metal capable of generating hydroxyl radicals that can oxidize DNA, and aluminum (Al) has been reported to facilitate Fe-mediated oxidation.
View Article and Find Full Text PDFJ Inorg Biochem
November 2009
Yumoto Institute of Neurology, Kawadacho 6-11, Shinjuku-ku, Tokyo 162-0054, Japan.
Aluminum (Al) exposure has been reported to be a risk factor for Alzheimer's disease (senile dementia of Alzheimer type), although the role of Al in the etiology of Alzheimer's disease remains controversial. We examined the presence of Al in the Alzheimer's brain using energy-dispersive X-ray spectroscopy combined with transmission electron microscopy (TEM-EDX). TEM-EDX analysis allows simultaneous imaging of subcellular structures with high spatial resolution and analysis of small quantities of elements contained in the same subcellular structures.
View Article and Find Full Text PDFJ Inorg Biochem
September 2003
Yumoto Institute of Neurology, Kawadacho 6-11, Shinjuku-ku, 162-0054 Tokyo, Japan.
Aluminium inhibits prenatal and postnatal brain development. However, aluminium incorporation into the brain of sucklings through maternal milk has not yet been well clarified because aluminium lacks a suitable isotope for radioactive tracer experiments. Using 26Al (26AlCl(3)) as a tracer, we measured 26Al incorporation into the brain of suckling rats by accelerator mass spectrometry.
View Article and Find Full Text PDFBrain Res Bull
May 2001
Yumoto Institute of Neurology, Tokyo, Japan.
Aluminium is highly neurotoxic and inhibits prenatal and postnatal development of the brain in humans and experimental animals. However, the incorporation of aluminium into the brain of fetuses and sucklings during gestation and lactation has not been well clarified because aluminium lacks a suitable isotope for a tracer experiment. In this study, we used 26Al (a radioisotope of aluminium with a half-life of 716,000 years) as a tracer, and measured 26Al incorporation into the brain of rat fetuses and sucklings by using accelerator mass spectrometry.
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