Physician
Pathology
Dr. Ashley I. Bush, MD
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Ashley Bush is an expert in the field of Pathology. Ashley Bush has written publications. He has 101 publications published with PubMed. The lastest publication is: 'Dramatic aggregation of Alzheimer abeta by Cu(II) is induced by conditions representing physiological acidosis.'
Publications
- Altered selenium status in Huntington's disease: Neuroprotection by selenite in the N171-82Q mouse model.
- Physical activity and amyloid-β plasma and brain levels: results from the Australian Imaging, Biomarkers and Lifestyle Study of Ageing.
- A blood-based predictor for neocortical Aβ burden in Alzheimer's disease: results from the AIBL study.
- The role of metallobiology and amyloid-? peptides in Alzheimer's disease.
- Dissociation of ERK signaling inhibition from the anti-amyloidogenic action of synthetic ceramide analogues.
- The Neurophysiology and Pathology of Brain Zinc.
- Elevated labile Cu is associated with oxidative pathology in Alzheimer disease.
- Homocysteine, Vitamin B12, and Folic Acid Levels in Alzheimer's Disease, Mild Cognitive Impairment, and Healthy Elderly: Baseline Characteristics in Subjects of the Au...
- The Alzheimer's therapeutic PBT2 promotes amyloid-β degradation and GSK3 phosphorylation via a metal chaperone activity.
- The efficacy of N-acetylcysteine as an adjunctive treatment in bipolar depression: An open label trial.
- Cysteine Oxidation within N-terminal Mutant Huntingtin Promotes Oligomerization and Delays Clearance of Soluble Protein.
- N-acetyl cysteine restores brain glutathione loss in combined 2-cyclohexene-1-one and d-amphetamine-treated rats: Relevance to schizophrenia and bipolar disorder.
- Presenilins promote the cellular uptake of copper and zinc and maintain copper chaperone of SOD1-dependent copper/zinc superoxide dismutase activity.
- Copper promotes the trafficking of the amyloid precursor protein.
- Copper modulation as a therapy for Alzheimer's disease?
- Metal ionophore treatment restores dendritic spine density and synaptic protein levels in a mouse model of Alzheimer's disease.
- Disturbed copper bioavailability in Alzheimer's disease.
- Interaction of glutathione depletion and psychotropic drug treatment in prepulse inhibition in rats and mice.
- Qualitative methods in early-phase drug trials: broadening the scope of data and methods from an RCT of N-acetylcysteine in schizophrenia.
- Iron-export ferroxidase activity of β-amyloid precursor protein is inhibited by zinc in Alzheimer's disease.
- Insulin-like signaling determines survival during stress via posttranscriptional mechanisms in C. elegans.
- Monomerized Cu, Zn-superoxide dismutase induces oxidative stress through aberrant Cu binding.
- Cognitive loss in zinc transporter-3 knock-out mice: a phenocopy for the synaptic and memory deficits of Alzheimer's disease?
- Kalzium ist nicht alles.
- Syntaxin 5 is required for copper homeostasis in Drosophila and mammals.
- The Caenorhabditis elegans A beta 1-42 model of Alzheimer disease predominantly expresses A beta 3-42.
- Paradoxical condensation of copper with elevated beta-amyloid in lipid rafts under cellular copper deficiency conditions: implications for Alzheimer disease.
- Chronic exposure to high levels of zinc or copper has little effect on brain metal homeostasis or Abeta accumulation in transgenic APP-C100 mice.
- Zinc and copper modulate Alzheimer Abeta levels in human cerebrospinal fluid.
- Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation.
- SLC30A3 responds to glucose- and zinc variations in beta-cells and is critical for insulin production and in vivo glucose-metabolism during beta-cell stress.
- Intracellular amyloid formation in muscle cells of Abeta-transgenic Caenorhabditis elegans: determinants and physiological role in copper detoxification.
- Sequestration of copper from beta-amyloid promotes selective lysis by cyclen-hybrid cleavage agents.
- N-acetyl cysteine for depressive symptoms in bipolar disorder--a double-blind randomized placebo-controlled trial.
- N-acetyl cysteine as a glutathione precursor for schizophrenia--a double-blind, randomized, placebo-controlled trial.
- Glutathione precursor, N-acetyl-cysteine, improves mismatch negativity in schizophrenia patients.
- Rapid restoration of cognition in Alzheimer's transgenic mice with 8-hydroxy quinoline analogs is associated with decreased interstitial Abeta.
- Therapeutics for Alzheimer's disease based on the metal hypothesis.
- Platinum-based inhibitors of amyloid-beta as therapeutic agents for Alzheimer's disease.
- Insights into Zn2+ homeostasis in neurons from experimental and modeling studies.
- Increased affinity for copper mediated by cysteine 111 in forms of mutant superoxide dismutase 1 linked to amyotrophic lateral sclerosis.
- Mechanisms of copper ion mediated Huntington's disease progression.
- Mitochondrial oxidative stress causes hyperphosphorylation of tau.
- Degradation of the Alzheimer disease amyloid beta-peptide by metal-dependent up-regulation of metalloprotease activity.
- Copper-mediated amyloid-beta toxicity is associated with an intermolecular histidine bridge.
- Gender and genetic background effects on brain metal levels in APP transgenic and normal mice: implications for Alzheimer beta-amyloid pathology.
- Hypoxia-inducible factor prolyl 4-hydroxylase inhibition. A target for neuroprotection in the central nervous system.
- Model studies of cholesterol and ascorbate oxidation by copper complexes: relevance to Alzheimer's disease beta-amyloid metallochemistry.
- Alzheimer disease beta-amyloid activity mimics cholesterol oxidase.
- Methylation of the imidazole side chains of the Alzheimer disease amyloid-beta peptide results in abolition of superoxide dismutase-like structures and inhibition of n...
- Mice transgenic for Alzheimer disease beta-amyloid develop lens cataracts that are rescued by antioxidant treatment.
- The integrated role of desferrioxamine and phenserine targeted to an iron-responsive element in the APP-mRNA 5'-untranslated region.
- The N-terminal copper-binding domain of the amyloid precursor protein protects against Cu2+ neurotoxicity in vivo.
- Enhanced toxicity and cellular binding of a modified amyloid beta peptide with a methionine to valine substitution.
- Genetically decreased spinal cord copper concentration prolongs life in a transgenic mouse model of amyotrophic lateral sclerosis.
- Tyrosine gated electron transfer is key to the toxic mechanism of Alzheimer's disease beta-amyloid.
- Serum copper: a biomarker for Alzheimer disease?
- Alzheimer's amyloid beta-peptide (1-42): involvement of methionine residue 35 in the oxidative stress and neurotoxicity properties of this peptide.
- Peroxidase activity of cyclooxygenase-2 (COX-2) cross-links beta-amyloid (Abeta) and generates Abeta-COX-2 hetero-oligomers that are increased in Alzheimer's disease.
- Neuronal zinc exchange with the blood vessel wall promotes cerebral amyloid angiopathy in an animal model of Alzheimer's disease.
- Estrogen decreases zinc transporter 3 expression and synaptic vesicle zinc levels in mouse brain.
- Redox-active metals, oxidative stress, and Alzheimer's disease pathology.
- Copper mediates dityrosine cross-linking of Alzheimer's amyloid-beta.
- Metal-protein attenuation with iodochlorhydroxyquin (clioquinol) targeting Abeta amyloid deposition and toxicity in Alzheimer disease: a pilot phase 2 clinical trial.
- Neurotoxic, redox-competent Alzheimer's beta-amyloid is released from lipid membrane by methionine oxidation.
- Copper, beta-amyloid, and Alzheimer's disease: tapping a sensitive connection.
- Current status of metals as therapeutic targets in Alzheimer's disease.
- Copper, zinc, and the metallobiology of Alzheimer disease.
- Genetic or pharmacological iron chelation prevents MPTP-induced neurotoxicity in vivo: a novel therapy for Parkinson's disease.
- Metal ions, pH, and cholesterol regulate the interactions of Alzheimer's disease amyloid-beta peptide with membrane lipid.
- Overexpression of Alzheimer's disease amyloid-beta opposes the age-dependent elevations of brain copper and iron.
- An iron-responsive element type II in the 5'-untranslated region of the Alzheimer's amyloid precursor protein transcript.
- Metal complexing agents as therapies for Alzheimer's disease.
- Metalloenzyme-like activity of Alzheimer's disease beta-amyloid. Cu-dependent catalytic conversion of dopamine, cholesterol, and biological reducing agents to neurotox...
- Is ALS caused by an altered oxidative activity of mutant superoxide dismutase?
- Alzheimer's disease drug discovery targeted to the APP mRNA 5'untranslated region.
- The galvanization of beta-amyloid in Alzheimer's disease.
- Could Abeta and AbetaPP be Antioxidants?
- A protease activity associated with acetylcholinesterase releases the membrane-bound form of the amyloid protein precursor of Alzheimer's disease.
- A novel zinc(II) binding site modulates the function of the beta A4 amyloid protein precursor of Alzheimer's disease.
- Zinc-induced Alzheimer's Abeta1-40 aggregation is mediated by conformational factors.
- Relative increase in Alzheimer's disease of soluble forms of cerebral Abeta amyloid protein precursor containing the Kunitz protease inhibitory domain.
- Dramatic aggregation of Alzheimer abeta by Cu(II) is induced by conditions representing physiological acidosis.
- Exacerbation of copper toxicity in primary neuronal cultures depleted of cellular glutathione.
- The A beta peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion reduction.
- The Alzheimer's disease amyloid precursor protein modulates copper-induced toxicity and oxidative stress in primary neuronal cultures.
- Aqueous dissolution of Alzheimer's disease Abeta amyloid deposits by biometal depletion.
- Pilot study of the reducing effect on amyloidosis in vivo by three FDA pre-approved drugs via the Alzheimer''s APP 5'' untranslated region.
- The amyloid beta-protein precursor and its mammalian homologues. Evidence for a zinc-modulated heparin-binding superfamily.
- The beta A4 amyloid protein precursor in human circulation.
- Modulation of A beta adhesiveness and secretase site cleavage by zinc.
- Differential effects of apolipoprotein E isoforms on metal-induced aggregation of A beta using physiological concentrations.
- Genetic studies of Alzheimer's disease: lessons learned and future imperatives.
- Specific metal-catalysed protein oxidation reactions in chronic degenerative disorders of ageing: focus on Alzheimer''s disease and age-related cataracts.
- Treatment with a copper-zinc chelator markedly and rapidly inhibits beta-amyloid accumulation in Alzheimer's disease transgenic mice.
- Copper catalyzed oxidation of Alzheimer Abeta.
- Amyloid plaques arise from zinc-enriched cortical layers in APP/PS1 transgenic mice and are paradoxically enlarged with dietary zinc deficiency.
- A role for glutathione in the pathophysiology of bipolar disorder and schizophrenia? Animal models and relevance to clinical practice.
- Beta A4 amyloid protein and its precursor in Alzheimer''s disease.
- Soluble pool of Abeta amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease.
Schools
University of Melbourne Faculty of Medicine
Austin Hospital
Royal Melbourne Hospital
Massachusetts General Hospital
Doctors Specialties
- Psychiatry
- Pathology
Accepted Insurances
Education
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University of Melbourne Faculty of Medicine
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