Robert D. Moir spends much of his time researching Biochemistry, Amyloid, Molecular biology, Lamin and Senile plaques. His research is interdisciplinary, bridging the disciplines of PBT2 and Biochemistry. His Amyloid research is multidisciplinary, incorporating perspectives in Ferroxidase activity, Ceruloplasmin, Transferrin and Copper.
His Molecular biology study combines topics from a wide range of disciplines, such as Endocytosis, Apolipoprotein E and Protein A. He has included themes like Enzyme, Cell nucleus, Poly ADP ribose polymerase and Cell biology in his Lamin study. His work carried out in the field of Senile plaques brings together such families of science as Cataracts, Lens protein and Pathogenesis.
His main research concerns Biochemistry, Amyloid, Disease, Cell biology and Alzheimer's disease. His Biochemistry research incorporates elements of PBT2, Zinc and P3 peptide, Amyloid precursor protein. His Amyloid research includes elements of Oxidative stress, Beta and Lens.
His study in Cell biology is interdisciplinary in nature, drawing from both Lamin and Intermediate filament. His study focuses on the intersection of Lamin and fields such as Molecular biology with connections in the field of Complementary DNA. As part of one scientific family, Robert D. Moir deals mainly with the area of Alzheimer's disease, narrowing it down to issues related to the Neuroscience, and often Neuropathology.
His scientific interests lie mostly in Disease, Alzheimer's disease, Neuroscience, Pathology and Innate immune system. His biological study spans a wide range of topics, including Oxidative stress, Antimicrobial, Immunology and Amyloidosis. Alzheimer's disease connects with themes related to Amyloid in his study.
His research in Amyloid intersects with topics in Amyloid beta and Biochemistry. His Biochemistry study frequently draws connections between adjacent fields such as Molecular biology. The various areas that Robert D. Moir examines in his Innate immune system study include Peptide and Virology.
Disease, Alzheimer's disease, Neuroscience, Amyloid and Innate immune system are his primary areas of study. His Disease study combines topics in areas such as Oxidative stress, Oxidation reduction, Pathogenesis, Photochemistry and Radical. His studies in Alzheimer's disease integrate themes in fields like Curcumin and Drosophila.
Robert D. Moir interconnects Long-term potentiation, Neuropathology, Neuroinflammation and Surgery in the investigation of issues within Neuroscience. His research integrates issues of Transferrin, Biochemistry, P3 peptide and Ferroxidase activity in his study of Amyloid. His Innate immune system study integrates concerns from other disciplines, such as Virology, Peptide and Amyloidosis.
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Treatment with a Copper-Zinc Chelator Markedly and Rapidly Inhibits β-Amyloid Accumulation in Alzheimer's Disease Transgenic Mice
Robert A Cherny;Craig S Atwood;Michel E Xilinas;Danielle N Gray.
The Aβ Peptide of Alzheimer's Disease Directly Produces Hydrogen Peroxide through Metal Ion Reduction†
Xudong Huang;Craig S. Atwood;Mariana A. Hartshorn;Gerd Multhaup.
Dramatic aggregation of Alzheimer abeta by Cu(II) is induced by conditions representing physiological acidosis.
C. S. Atwood;R. D. Moir;Xudong Huang;R. C. Scarpa.
Journal of Biological Chemistry (1998)
Cu(II) Potentiation of Alzheimer Aβ Neurotoxicity CORRELATION WITH CELL-FREE HYDROGEN PEROXIDE PRODUCTION AND METAL REDUCTION
Xudong Huang;Math P. Cuajungco;Craig S. Atwood;Mariana A. Hartshorn.
Journal of Biological Chemistry (1999)
Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model.
Lee E. Goldstein;Andrew M. Fisher;Chad A. Tagge;Xiao-Lei Zhang.
Science Translational Medicine (2012)
Characterization of copper interactions with alzheimer amyloid beta peptides: identification of an attomolar-affinity copper binding site on amyloid beta1-42.
Craig S. Atwood;Richard C. Scarpa;Xudong Huang;Robert D. Moir.
Journal of Neurochemistry (2008)
Metalloenzyme-like Activity of Alzheimer's Disease β-Amyloid Cu-DEPENDENT CATALYTIC CONVERSION OF DOPAMINE, CHOLESTEROL, AND BIOLOGICAL REDUCING AGENTS TO NEUROTOXIC H2O2
Carlos Opazo;Xudong Huang;Robert A. Cherny;Robert D. Moir.
Journal of Biological Chemistry (2002)
Nuclear lamins: building blocks of nuclear architecture
Robert D. Goldman;Yosef Gruenbaum;Yosef Gruenbaum;Robert D. Moir;Dale K. Shumaker.
Genes & Development (2002)
Iron-Export Ferroxidase Activity of β-Amyloid Precursor Protein Is Inhibited by Zinc in Alzheimer's Disease
James A. Duce;Andrew Tsatsanis;Michael A. Cater;Simon A. James.
Alzheimer-associated presenilins 1 and 2: Neuronal expression in brain and localization to intracellular membranes in mammalian cells
Dora M. Kovacs;Hillary J. Fausett;Keith J. Page;Tae Wan Kim.
Nature Medicine (1996)
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