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The metal ion hypothesis of Alzheimer?s disease and the anti-neuroinflammatory effect of metal chelators

BIOORGANIC CHEMISTRY (2023)

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Arnab Kumar Nath et al.

Summary: Amyloid imbalance and A beta plaque formation are key features of Alzheimer's disease. The plaques contain increased levels of Cu and deposition of the heme cofactor, suggesting a possible association of the metal and cofactor in the pathology. Heme and Cu bind with A beta separately to form heme-A beta and Cu-A beta complexes, and they can also bind simultaneously to generate a heme-Cu-A beta complex.

DALTON TRANSACTIONS (2022)

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Article Neurosciences

α-Lipoic Acid Has the Potential to Normalize Copper Metabolism, Which Is Dysregulated in Alzheimer's Disease

Kristel Metsla et al.

Summary: This study found that alpha-lipoic acid (LA) can translocate copper from the extracellular to intracellular space, alleviating the intracellular copper deficit characteristic of Alzheimer's disease (AD) neurons. Additionally, LA can protect Drosophila melanogaster AD models from AD phenotype development and improve locomotor activity in fruit flies with overexpression of human A beta in the fly brain. These results suggest that LA has the potential to normalize copper metabolism in AD.

JOURNAL OF ALZHEIMERS DISEASE (2022)

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Article Biochemical Research Methods

Uncovering the Metabolic Mechanism of Salidroside AlleviatingMicroglial Hypoxia Inflammation Based on Microfluidic Chip-MassSpectrometry

Fangfang Fan et al.

Summary: This study elucidated a new mechanism of Salidroside in reducing hypoxia-induced inflammation in microglia by regulating cellular energy metabolism. The hypoxic microenvironment of BV2 microglial cells was simulated in vitro using a cell microfluidic chip-mass spectrometry (CM-MS) system, and the real-time change of cell metabolites was investigated. The levels of hypoxia-related factors were also detected to confirm the metabolic mechanism of BV2 cells under hypoxia. The study found that Salidroside could invert the changes in cellular energy metabolism and identified two metabolites of Salidroside.

JOURNAL OF PROTEOME RESEARCH (2022)

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Article Biochemistry & Molecular Biology

Eriodictyol ameliorates cognitive dysfunction in APP/PS1 mice by inhibiting ferroptosis via vitamin D receptor-mediated Nrf2 activation

Lin Li et al.

Summary: Eriodictyol alleviates memory impairment and AD-like pathological changes by activating the Nrf2/HO-1 signaling pathway through a mechanism mediated by VDR.

MOLECULAR MEDICINE (2022)

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Article Neurosciences

Ferroptosis promotes microtubule-associated protein tau aggregation via GSK-3 beta activation and proteasome inhibition

Shaohui Wang et al.

Summary: This study demonstrates that ferroptosis promotes abnormal aggregation of tau protein and may serve as a promising therapeutic target for tauopathies.

MOLECULAR NEUROBIOLOGY (2022)

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Article Neurosciences

Desferrioxamine Ameliorates Lipopolysaccharide-Induced Lipocalin-2 Upregulation via Autophagy Activation in Primary Astrocytes

Juntao Cui et al.

Summary: In this study, it was discovered that iron chelator deferoxamine (DFO) can inhibit the upregulation of Lipocalin-2 (LCN2) in astrocytes, independent of iron overload. This inhibitory effect is similar to that of autophagy inducers and does not rely on the proteasome system or the NF-kappa B pathway. DFO also promotes secretory autophagy, which improves the upregulation of LCN2 in astrocytes.

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Activation of vitamin D receptor inhibits Tau phosphorylation is associated with reduction of iron accumulation in APP/PS1 transgenic mice

Ting-Yao Wu et al.

Summary: This study found that activation of the vitamin D receptor (VDR) can reduce iron accumulation and phosphorylated Tau and β-amyloid (Aβ) deposition in the brains of Alzheimer's disease (AD) through downregulating transferrin receptor (TFR) expression, suggesting that activation of VDR may be an effective strategy for treating AD.

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TREM2 and CD163 Ameliorate Microglia-Mediated Inflammatory Environment in the Aging Brain

Xue Han et al.

Summary: This study explored the expression of age-related genes in the human hippocampus using microarray data. The results identified two genes, TREM2 and CD163, which were significantly upregulated in aged mice. In addition, the levels of inflammatory factors were increased. These findings suggest that TREM2 and CD163 may play a role in delaying cognitive decline by alleviating the inflammatory environment in the aging brain.

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Alpha-lipoic acid improved motor function in MPTP-induced Parkinsonian mice by reducing neuroinflammation in the nigral and spinal cord

Jian Zhang et al.

Summary: This study investigated the effect of alpha-lipoic acid (ALA) on neuroinflammation and motor function in a mouse model of Parkinson's disease (PD). The results showed that ALA treatment could reduce the activation of microglia, decrease neuroinflammation, and improve motor function.

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Copper induces cell death by targeting lipoylated TCA cycle proteins

Peter Tsvetkov et al.

Summary: Copper is an essential cofactor for all organisms, but excessive copper can lead to cell death. We found that copper-dependent cell death mechanism is different from known mechanisms, and it is related to mitochondrial respiration. Copper directly binds to lipoylated components of the tricarboxylic acid cycle, causing protein aggregation and loss of iron-sulfur cluster proteins, ultimately leading to cell death.

SCIENCE (2022)

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Rationally Designed Molecules Synergistically Modulate Multifaceted Aβ Toxicity, Microglial Activation, and Neuroinflammation

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Summary: Synergistic modulation of multifaceted toxicity is crucial for tackling multifactorial Alzheimer's disease. In this study, a multifunctional modulator was designed by integrating pharmacophores for metal chelation, antioxidant and anti-inflammatory properties, and modulation of amyloid aggregation. The modulator showed promising results in vitro and cellular studies, effectively reducing amyloid toxicity, scavenging reactive oxygen species, alleviating oxidative stress, and inhibiting neuroinflammation. The study highlights the importance of integrating multiple pharmacophores to address the complex toxicity of Alzheimer's disease.

ACS CHEMICAL NEUROSCIENCE (2022)

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Copper induces microglia-mediated neuroinflammation through ROS/ NF-?B pathway and mitophagy disorder

Qian Zhou et al.

Summary: This study investigates the effects of copper exposure on microglial activation and neuroinflammation, as well as the underlying mechanism of copper-induced microglial activation. The results show that copper exposure leads to inflammatory activation of microglia and the release of inflammatory factors, which results in the death of dopaminergic neurons.

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Article Chemistry, Inorganic & Nuclear

Azo-Stilbene and Pyridine-Amine Hybrid Multifunctional Molecules to Target Metal-Mediated Neurotoxicity and Amyloid-β Aggregation in Alzheimer's Disease

Monika Rana et al.

Summary: This study focuses on the design and synthesis of two compounds, AS-HL1 and AS-HL2, which exhibit multifunctional properties including metal chelation ability, regulation of amyloid-beta aggregation pathways, scavenging free radicals, inhibiting acetylcholinesterase activity, and reducing cytotoxicity. These compounds also show promising potential for the treatment of Alzheimer's disease.

INORGANIC CHEMISTRY (2022)

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Impact of N-Truncated Aβ Peptides on Cu- and Cu(Aβ)-Generated ROS: CuI Matters!

Charlene Esmieu et al.

Summary: The study found that N-truncated peptides of Aβ are able to produce ROS in the presence of Cu-I, although to a lesser extent compared to unmodified peptides, and they are unable to fully prevent Cu(Aβ(1-16))-induced ROS production as competitor ligands.

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Loss of ferroportin induces memory impairment by promoting ferroptosis in Alzheimer's disease

Wen-Dai Bao et al.

Summary: Iron homeostasis disturbance and ferroptosis play critical roles in the pathogenesis and progression of Alzheimer's disease, and targeting these processes may provide promising therapeutic approaches for this disease.

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Unexpected Trends in Copper Removal from Aβ Peptide: When Less Ligand Is Better and Zn Helps

Charlene Esmieu et al.

Summary: Copper, zinc, and amyloid-beta peptides are crucial in the etiology of Alzheimer's disease, affecting the formation of amyloid plaques. The use of a phenanthroline-based ligand can withdraw copper from A beta and stabilize it in a 4N Cu(II) binding site, but excess ligand can decrease the prevention of ROS production, which is counteracted by the presence of zinc ions.

INORGANIC CHEMISTRY (2021)

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Novel sampangine derivatives as potent inhibitors of Cu2+-mediated amyloid-β protein aggregation, oxidative stress and inflammation

Xiao-yan Zou et al.

Summary: A series of 11-substituted sampangine derivatives were designed, synthesized, and tested for their ability to inhibit cholinesterase. Among them, compound 11 showed strong anti-acetylcholinesterase activity, high blood-brain barrier penetration ability, and high binding affinity to Cu2+. Additional experiments demonstrated that compound 11 suppressed the formation of Cu2+-A beta complexes, alleviated Cu2+ induced neurotoxicity, and inhibited the production of ROS catalyzed by Cu2+ in A beta 42 transgenic C elegans. Furthermore, compound 11 also inhibited the expressions of proinflammatory cytokines induced by Cu2+ + A beta(1-42) in BV2 microglial cells.

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SFRP1 modulates astrocyte-to-microglia crosstalk in acute and chronic neuroinflammation

Javier Rueda-Carrasco et al.

Summary: Neuroinflammation is a common feature of many neurodegenerative diseases. SFRP1, a multifunctional regulator of cell-to-cell communication, plays a role in promoting and sustaining microglial activation in mouse models of acute and chronic neuroinflammation, representing a potential therapeutic target for counteracting chronic inflammation in neurodegenerative diseases.

EMBO REPORTS (2021)

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Review Clinical Neurology

Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?

Fangda Leng et al.

Summary: Microglial activation and neuroinflammation play important roles in Alzheimer's disease, affecting disease progression and pathologies. Current research focuses on the interplay between neuroinflammation and amyloid and tau pathologies, with a specific interest in modulating microglia as a therapeutic strategy for AD.

NATURE REVIEWS NEUROLOGY (2021)

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Article Neurosciences

Elevated neuroinflammation contributes to the deleterious impact of iron overload on brain function in aging

Alireza Salami et al.

Summary: Research shows that brain iron content increases nonlinearly with age and has complex associations with brain activity. Neuroinflammation partially mediates the impact of iron on brain activity. These findings enhance our understanding of how iron may negatively affect brain function and cognition.

NEUROIMAGE (2021)

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Article Multidisciplinary Sciences

Filamentous recombinant human Tau activates primary astrocytes via an integrin receptor complex

Peng Wang et al.

Summary: Microtubule-associated protein Tau can form protein aggregates transmissible within the brain, correlating with the progression of tauopathies in humans. The entry of filamentous recombinant human Tau into astrocytes via the integrin alpha V/beta 1 complex stimulates integrin signaling, resulting in activation of NF kappa B and astrocyte conversion towards a neurotoxic state.

NATURE COMMUNICATIONS (2021)

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Article Neurosciences

Iron Responsive Element-Mediated Responses to Iron Dyshomeostasis in Alzheimer's Disease

Nhi Hin et al.

Summary: IRE gene expression changes serve as early markers of the pathogenic process in fAD, highlighting iron dyshomeostasis as a significant driver of the disease. The differences in the stability of IRE-containing transcripts can be utilized to explore and compare iron dyshomeostasis-associated gene expression responses across various species, tissues, and conditions.

JOURNAL OF ALZHEIMERS DISEASE (2021)

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Protective role of microglial HO-1 blockade in aging: Implication of iron metabolism

Cristina Fernandez-Mendivil et al.

Summary: The study revealed that overexpression of HO-1 in microglial cells in aged mice leads to neurotoxic iron accumulation, oxidative stress, and cognitive decline. Inhibiting HO-1 or using an iron chelator can prevent these issues, providing new insights for treating age-related neurodegenerative diseases.

REDOX BIOLOGY (2021)

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Article Biochemistry & Molecular Biology

Hybrid Bis-Histidine Phenanthroline-Based Ligands to Lessen Aβ-Bound Cu ROS Production: An Illustration of Cu(I) Significance

Marielle Drommi et al.

Summary: This study reports the synthesis of three new hybrid ligands designed to capture copper from amyloid-beta peptides and prevent the formation of reactive oxygen species. The research investigated the copper complexes formed with the ligands and their ability to remove copper from A beta, highlighting the importance of the reduced state of copper (Cu(I) in preventing and inhibiting reactive oxygen species.

MOLECULES (2021)

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Iron loading is a prominent feature of activated microglia in Alzheimer's disease patients

Boyd Kenkhuis et al.

Summary: Brain iron accumulation accelerates disease progression in Alzheimer patients with amyloid-beta. Activated microglia with increased iron accumulation influence the functional phenotype of cells, especially in conjunction with amyloid-beta. Spatial analysis showed that iron-accumulating microglia predominantly infiltrated A beta-plaques in the brain.

ACTA NEUROPATHOLOGICA COMMUNICATIONS (2021)

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Curcumin Reduces Cognitive Deficits by Inhibiting Neuroinflammation through the Endoplasmic Reticulum Stress Pathway in Apolipoprotein E4 Transgenic Mice

Jiejian Kou et al.

Summary: The study found that curcumin can reduce the high expression of ApoE4 and excessive release of inflammatory factors in ApoE4 transgenic mice, improving cognitive ability by inhibiting endoplasmic reticulum stress.

ACS OMEGA (2021)

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Metallobiology and therapeutic chelation of biometals (copper, zinc and iron) in Alzheimer's disease: Limitations, and current and future perspectives

Kehinde D. Fasae et al.

Summary: Alzheimer's disease is the leading cause of cognitive impairment and dementia globally, with various hypotheses on its pathobiology but no confirmed diagnostics or approved cure. Studies suggest that imbalances in biometal ions and metal-amyloid interactions play crucial roles in AD pathogenesis, highlighting the importance of therapeutic chelation strategies in reducing cerebral metal burden and inhibiting A beta aggregation. Developments in multi-target ligands as potential anti-AD drug candidates show promise in addressing the limitations of current drug candidates and improving chelation-based therapeutics for AD.

JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY (2021)

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A Water-Soluble Peptoid Chelator that Can Remove Cu2+ from Amyloid-β Peptides and Stop the Formation of Reactive Oxygen Species Associated with Alzheimer's Disease

Anastasia E. Behar et al.

Summary: The study introduces a water-soluble peptidomimetic chelator, P3, that selectively removes Cu2+ from Cu-Aβ and prevents the formation of ROS, showing potential advantages in the treatment of AD.

ANGEWANDTE CHEMIE-INTERNATIONAL EDITION (2021)

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Aducanumab: First Approval

Sohita Dhillon

Summary: Aducanumab is a monoclonal antibody developed for the treatment of Alzheimer's disease, targeting aggregated forms of amyloid beta. It has received approval in the USA for use in patients with mild cognitive impairment or mild dementia. Ongoing studies are evaluating its safety and efficacy in patients with early Alzheimer's disease.

DRUGS (2021)

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Alpha lipoic acid ameliorates scopolamine induced memory deficit and neurodegeneration in the cerebello-hippocampal cortex

Adejoke Elizabeth Memudu et al.

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METABOLIC BRAIN DISEASE (2021)

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Copper-Binding Peptides Attenuate Microglia Inflammation through Suppression of NF-kB Pathway

Maria Elisa Caetano-Silva et al.

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Astrocytic interleukin-3 programs microglia and limits Alzheimer's disease

Cameron S. McAlpine et al.

Summary: Communication within the glial cell ecosystem is essential for neuronal and brain health. This study demonstrates that astrocyte-sourced interleukin-3 programs microglia to ameliorate the pathology of Alzheimer's disease by enhancing their ability to clear aggregates of beta-amyloid and tau, ultimately restricting disease progression and cognitive decline. These findings highlight IL-3 as a key mediator of astrocyte-microglia cross-talk and a potential therapeutic target for Alzheimer's disease.

NATURE (2021)

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Microglial activation and tau propagate jointly across Braak stages

Tharick A. Pascoal et al.

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NATURE MEDICINE (2021)

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Sanghamitra Bandyopadhyay

Summary: This paragraph discusses the key roles of amyloidogenicity and vascular dysfunction in the pathogenesis of Alzheimer's disease, focusing on the dysregulated cellular interactions between neurons, glial cells, and vascular cells. It highlights how cerebrovascular diseases overlap neuropathologically with AD, and how glial dyshomeostasis contributes to the neurodegenerative cascade in AD.

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Copper Imbalance in Alzheimer's Disease: Meta-Analysis of Serum, Plasma, and Brain Specimens, and Replication Study Evaluating ATP7B Gene Variants

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Prolonged exposure of cortical neurons to oligomeric amyloid-beta impairs NMDA receptor function via NADPH oxidase-mediated ROS production: protective effect of green tea (-)-epigallocatechin-3-gallate

Yan He et al.

ASN NEURO (2011)

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Review Clinical Neurology

Metal attenuating therapies in neurodegenerative disease

Alexandra I. Mot et al.

EXPERT REVIEW OF NEUROTHERAPEUTICS (2011)

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Article Genetics & Heredity

The Alzheimer's amyloid β-peptide (Aβ) binds a specific DNA Aβ-interacting domain (AβID) in the APP, BACE1, and APOE promoters in a sequence-specific manner: Characterizing a new regulatory motif

Bryan Maloney et al.

GENE (2011)

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Article Neurosciences

Tau Protein Is Required for Amyloid β-Induced Impairment of Hippocampal Long-Term Potentiation

Olivia A. Shipton et al.

JOURNAL OF NEUROSCIENCE (2011)

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Review Biochemistry & Molecular Biology

Role of metal dyshomeostasis in Alzheimer's disease

David J. Bonda et al.

METALLOMICS (2011)

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Article Clinical Neurology

Beneficial effect of human anti-amyloid-β active immunization on neurite morphology and tau pathology

Alberto Serrano-Pozo et al.

BRAIN (2010)

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Article Cell Biology

Up-regulation of divalent metal transporter 1 in 6-hydroxydopamine intoxication is IRE/IRP dependent

Hong Jiang et al.

CELL RESEARCH (2010)

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Article Food Science & Technology

Hepatotoxicity of high oral dose (-)-epigallocatechin-3-gallate in mice

Joshua D. Lambert et al.

FOOD AND CHEMICAL TOXICOLOGY (2010)

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Review Chemistry, Medicinal

Mechanisms of brain iron transport: insight into neurodegeneration and CNS disorders

Eric Mills et al.

FUTURE MEDICINAL CHEMISTRY (2010)

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Article Neurosciences

NMR Studies of Zinc, Copper, and Iron Binding to Histidine, the Principal Metal Ion Complexing Site of Amyloid-beta Peptide

Nanditha G. Nair et al.

JOURNAL OF ALZHEIMERS DISEASE (2010)

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Article Neurosciences

PBT2 Rapidly Improves Cognition in Alzheimer's Disease: Additional Phase II Analyses

Noel G. Faux et al.

JOURNAL OF ALZHEIMERS DISEASE (2010)

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Article Biochemistry & Molecular Biology

Substoichiometric Levels of Cu2+ Ions Accelerate the Kinetics of Fiber Formation and Promote Cell Toxicity of Amyloid-β from Alzheimer Disease

Claire J. Sarell et al.

JOURNAL OF BIOLOGICAL CHEMISTRY (2010)

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Article Neurosciences

Aβ Oligomers Cause Localized Ca2+ Elevation, Missorting of Endogenous Tau into Dendrites, Tau Phosphorylation, and Destruction of Microtubules and Spines

Hans Zempel et al.

JOURNAL OF NEUROSCIENCE (2010)

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Article Multidisciplinary Sciences

Zinc Overload Enhances APP Cleavage and Aβ Deposition in the Alzheimer Mouse Brain

Chun-Yan Wang et al.

PLOS ONE (2010)

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Article Multidisciplinary Sciences

EGCG remodels mature α-synuclein and amyloid-β fibrils and reduces cellular toxicity

Jan Bieschke et al.

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2010)

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Article Immunology

Trace amounts of copper exacerbate beta amyloid-induced neurotoxicity in the cholesterol-fed mice through TNF-mediated inflammatory pathway

Jun Lu et al.

BRAIN BEHAVIOR AND IMMUNITY (2009)

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Article Radiology, Nuclear Medicine & Medical Imaging

MRI and Histological Analysis of Beta-Amyloid Plaques in Both Human Alzheimer's Disease and APP/PS1 Transgenic Mice

Mark D. Meadowcroft et al.

JOURNAL OF MAGNETIC RESONANCE IMAGING (2009)

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Correction Clinical Neurology

Safety, efficacy, and biomarker findings of PBT2 in targeting Aβ as a modifying therapy for Alzheimer's disease: a phase IIa, double-blind, randomised, placebo-controlled trial (vol 7, pg 779, 2008)

L. Lannfelt et al.

LANCET NEUROLOGY (2009)

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Review Biochemistry & Molecular Biology

Intracellular iron transport and storage: From molecular mechanisms to health implications

Elizabeth L. Mackenzie et al.

ANTIOXIDANTS & REDOX SIGNALING (2008)

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Review Neurosciences

Physiological and pathological aspects of Aβ in iron homeostasis via 5′UTR in the APP mRNA and the therapeutic use of iron-chelators

Yael Avramovich-Tirosh et al.

BMC NEUROSCIENCE (2008)

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Article Neurosciences

Zinc triggers microglial activation

Tiina M. Kauppinen et al.

JOURNAL OF NEUROSCIENCE (2008)

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Article Chemistry, Multidisciplinary

The Amyloid-β Peptide of Alzheimer's Disease Binds CuI in a Linear Bis-His Coordination Environment: Insight into a Possible Neuroprotective Mechanism for the Amyloid-β Peptide

Jason Shearer et al.

JOURNAL OF THE AMERICAN CHEMICAL SOCIETY (2008)

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Article Neurosciences

Rapid restoration of cognition in Alzheimer's transgenic mice with 8-hydroxy quinoline analogs is associated with decreased interstitial Aβ

Paul A. Adlard et al.

NEURON (2008)

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Article Clinical Neurology

Safety, efficacy, and biomarker findings of PBT2 in targeting Aβ as a modifying therapy for Alzheimer's disease:: a phase IIa, double-blind, randomised, placebo-controlled trial

Lars Lannfelt et al.

LANCET NEUROLOGY (2008)

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Article Biochemistry & Molecular Biology

Three histidine residues of amyloid-β peptide control the redox activity of copper and iron

M. Nakamura et al.

BIOCHEMISTRY (2007)

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Article Biochemistry & Molecular Biology

Zinc lowers amyloid-β toxicity by selectively precipitating aggregation intermediates

K. Garai et al.

BIOCHEMISTRY (2007)

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Article Neurosciences

Aβ oligomer-induced aberrations in synapse composition, shape, and density provide a molecular basis for loss of connectivity in Alzheimer's disease

Pascale N. Lacor et al.

JOURNAL OF NEUROSCIENCE (2007)

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Article Biophysics

Time-dependent DNA condensation induced by amyloid beta-peptide

Haijia Yu et al.

BIOPHYSICAL JOURNAL (2007)

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Article Clinical Neurology

Copper deficiency elicits glial and neuronal response typical of neurodegenerative disorders

G. G. Zucconi et al.

NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY (2007)

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Article Neurosciences

Cellular iron status influences the functional relationship between microglia and Oligodendrocytes

X. Zhang et al.

GLIA (2006)

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Article Clinical Neurology

Elevated cortical zinc in Alzheimer disease

D. Religa et al.

NEUROLOGY (2006)

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Article Biochemistry & Molecular Biology

Synchrotron-based infrared and X-ray imaging shows focalized accumulation of Cu and Zn co-localized with β-amyloid deposits in Alzheimer's disease

Lisa M. Miller et al.

JOURNAL OF STRUCTURAL BIOLOGY (2006)

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Article Multidisciplinary Sciences

A specific amyloid-β protein assembly in the brain impairs memory

S Lesné et al.

NATURE (2006)

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Article Biochemistry & Molecular Biology

Redox cycling of iron by Aβ42

A Khan et al.

FREE RADICAL BIOLOGY AND MEDICINE (2006)

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Review Neurosciences

Astrocyte-endothelial interactions at the blood-brain barrier

NJ Abbott et al.

NATURE REVIEWS NEUROSCIENCE (2006)

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Article Biochemistry & Molecular Biology

Copper binding to the amyloid-β (Aβ) peptide associated with Alzheimer's disease -: Folding, coordination geometry, pH dependence, stoichiometry, and affinity of Aβ-(1-28):: Insights from a range of complementary spectroscopic techniques

CD Syme et al.

JOURNAL OF BIOLOGICAL CHEMISTRY (2004)

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Article Neurosciences

Alterations in human tau transcripts correlate with those of neurofilament in sporadic tauopathies

Y Umeda et al.

NEUROSCIENCE LETTERS (2004)

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Article Biochemistry & Molecular Biology

RAGE mediates amyloid-β peptide transport across the blood-brain barrier and accumulation in brain

R Deane et al.

NATURE MEDICINE (2003)

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Review Neurosciences

The metallobiology of Alzheimer's disease

AI Bush

TRENDS IN NEUROSCIENCES (2003)

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Article Biochemistry & Molecular Biology

Copper reduction by copper binding proteins and its relation to neurodegenerative diseases

C Opazo et al.

BIOMETALS (2003)

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Article Clinical Neurology

Metal-protein attenuation with iodochlorhydroxyquin (clioquinol) targeting A beta amyloid deposition and toxicity in Alzheimer disease - A pilot phase 2 clinical trial

CW Ritchie et al.

ARCHIVES OF NEUROLOGY (2003)

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Review Neurosciences

Zinc takes the center stage: its paradoxical role in Alzheimer's disease

MP Cuajungco et al.

BRAIN RESEARCH REVIEWS (2003)

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Article Biochemistry & Molecular Biology

Metalloenzyme-like activity of Alzheimer's disease β-amyloid -: Cu-dependent catalytic conversion of dopamine, cholesterol, and biological reducing agents to neurotoxic H2O2

C Opazo et al.

JOURNAL OF BIOLOGICAL CHEMISTRY (2002)

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Article Clinical Neurology

Phases of Aβ-deposition in the human brain and its relevance for the development of AD

DR Thal et al.

NEUROLOGY (2002)

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Article Biochemistry & Molecular Biology

Zinc enhances synthesis of presenilin 1 in mouse primary cortical culture

IH Park et al.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2001)

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Article Neurosciences

Treatment with a copper-zinc chelator markedly and rapidly inhibits β-amyloid accumulation in Alzheimer's disease transgenic mice

RA Cherny et al.

NEURON (2001)

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Article Biochemistry & Molecular Biology

Redox-active iron mediates amyloid-β toxicity

CA Rottkamp et al.

FREE RADICAL BIOLOGY AND MEDICINE (2001)

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Article Gastroenterology & Hepatology

Localisation of divalent metal transporter I (DMT1) to the microvillus membrane of rat duodenal enterocytes in iron deficiency, but to hepatocytes in iron overload

D Trinder et al.

GUT (2000)

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