Chronic copper exposure exacerbates both amyloid and tau pathology and selectively dysregulates cdk5 in a mouse model of AD

Triple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles

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Copper, iron and zinc in Alzheimer's disease senile plaques

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Treatment with a Copper-Zinc Chelator Markedly and Rapidly Inhibits β-Amyloid Accumulation in Alzheimer's Disease Transgenic Mice

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Neurotoxicity induces cleavage of p35 to p25 by calpain

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Dramatic Aggregation of Alzheimer Aβ by Cu(II) Is Induced by Conditions Representing Physiological Acidosis

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Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration <i>in vivo</i>

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Lipopolysaccharide-Induced Inflammation Exacerbates Tau Pathology by a Cyclin-Dependent Kinase 5-Mediated Pathway in a Transgenic Model of Alzheimer's Disease

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Characterization of Copper Interactions with Alzheimer Amyloid β Peptides: Identification of an Attomolar‐Affinity Copper Binding Site on Amyloid β1‐42

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Glucocorticoids increase amyloid-β and tau pathology in a mouse model of alzheimer’s disease

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Aberrant Cdk5 activation by p25 triggers pathological events leading to neurodegeneration and neurofibrillary tangles

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Trace amounts of copper in water induce β-amyloid plaques and learning deficits in a rabbit model of Alzheimer's disease

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Contribution by synaptic zinc to the gender-disparate plaque formation in human Swedish mutant APP transgenic mice

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Increased level of active GSK‐3β in Alzheimer’s disease and accumulation in argyrophilic grains and in neurones at different stages of neurofibrillary degeneration

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β-Site Amyloid Precursor Protein Cleaving Enzyme 1 Levels Become Elevated in Neurons around Amyloid Plaques: Implications for Alzheimer's Disease Pathogenesis

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Dimeric Amyloid β Protein Rapidly Accumulates in Lipid Rafts followed by Apolipoprotein E and Phosphorylated Tau Accumulation in the Tg2576 Mouse Model of Alzheimer's Disease

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Overexpression of Alzheimer's Disease Amyloid-β Opposes the Age-dependent Elevations of Brain Copper and Iron

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Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice

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Copper levels are increased in the cerebral cortex and liver of APP and APLP2 knockout mice

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Structure of the Alzheimer's Disease Amyloid Precursor Protein Copper Binding Domain

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Dietary Copper and High Saturated and trans Fat Intakes Associated With Cognitive Decline

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The Alzheimer's Disease Amyloid Precursor Protein Modulates Copper-Induced Toxicity and Oxidative Stress in Primary Neuronal Cultures

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Binding of zinc(II) and copper(II) to the full‐length Alzheimer’s amyloid‐β peptide

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Alternative splicing isoform of tau protein kinase I/glycogen synthase kinase 3β

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In vivo reduction of amyloid-β by a mutant copper transporter

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Glycogen synthase kinase-3 is associated with neuronal and glial hyperphosphorylated tau deposits in Alzheimer's disease, Pick's disease, progressive supranuclear palsy and corticobasal degeneration

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Imaging and spatial distribution of β-amyloid peptide and metal ions in Alzheimer’s plaques by laser ablation–inductively coupled plasma–mass spectrometry

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Copper inhibits β -amyloid production and stimulates the non-amyloidogenic pathway of amyloid-precursor-protein secretion

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Clioquinol Mediates Copper Uptake and Counteracts Copper Efflux Activities of the Amyloid Precursor Protein of Alzheimer's Disease

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BACE1 Cytoplasmic Domain Interacts with the Copper Chaperone for Superoxide Dismutase-1 and Binds Copper

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Copper, Zinc, and the Metallobiology of Alzheimer Disease

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Exposure to metal ions regulates mRNA levels of APP and BACE1 in PC12 cells: Blockage by curcumin

Lin, R., Chen, X., Li, W., Han, Y., Liu, P., & Pi, R. (2008) · Neuroscience Letters · doi:10.1016/j.neulet.2008.05.070 · Cited by 114 · see citing works

Gene expression profiling in chronic copper overload reveals upregulation ofPrnpandApp

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Colocalization and Fluorescence Resonance Energy Transfer between cdk5 and AT8 Suggests a Close Association in Pre-Neurofibrillary Tangles and Neurofibrillary Tangles

Augustinack, J. C., Sanders, J. L., Tsai, L., & Hyman, B. T. (2002) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/61.6.557 · Cited by 72 · see citing works

Trace amounts of copper induce neurotoxicity in the cholesterol‐fed mice through apoptosis

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Identification of a novel high affinity copper binding site in the APP(145–155) fragment of amyloid precursor protein

Valensin, D., Mancini, F. M., Łuczkowski, M., et al. (2003) · Dalton Transactions · doi:10.1039/b312411h · Cited by 53 · see citing works

Copper and clioquinol treatment in young APP transgenic and wild-type mice: effects on life expectancy, body weight, and metal-ion levels

Schäfer, S., Pajonk, F., Multhaup, G., & Bayer, T. A. (2007) · Journal of Molecular Medicine · doi:10.1007/s00109-006-0140-7 · Cited by 47 · see citing works

Aβ peptide conformation determines uptake and interleukin-1α expression by primary microglial cells

Parvathy, S., Rajadas, J., Ryan, H. S., Vaziri, S., Anderson, L., & Murphy, G. M. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.01.011 · Cited by 39 · see citing works

Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease

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Ceramides in Alzheimer’s Disease: Key Mediators of Neuronal Apoptosis Induced by Oxidative Stress and A <b> <i>β</i> </b> Accumulation

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Metals and Neuronal Metal Binding Proteins Implicated in Alzheimer’s Disease

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Modulation of tau phosphorylation by environmental copper

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Exposure of metal toxicity in Alzheimer’s disease: An extensive review

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Amyloid β-interacting partners in Alzheimer's disease: From accomplices to possible therapeutic targets

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Role of Tau Protein in Neurodegenerative Diseases and Development of Its Targeted Drugs: A Literature Review

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The role of copper and the copper-related protein CUTA in mediating APP processing and Aβ generation

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Aging Increased Amyloid Peptide and Caused Amyloid Plaques in Brain of Old APP/V717I Transgenic Mice by a Different Mechanism than Mutant Presenilin1

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Modeling Alzheimer's disease in transgenic mice: effect of age and of Presenilin1 on amyloid biochemistry and pathology in APP/London mice

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Reversal of Alzheimer’s-like pathology and behavior in human APP transgenic mice by mutation of Asp664

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Expression of human FE65 in amyloid precursor protein transgenic mice is associated with a reduction in β‐amyloid load

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Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins

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