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8 hydroxyquinoline/atrophie
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Different 8-hydroxyquinolines protect models of TDP-43 protein, α-synuclein, and polyglutamine proteotoxicity through distinct mechanisms.
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No current therapies target the underlying cellular pathologies of age-related neurodegenerative diseases. Model organisms provide a platform for discovering compounds that protect against the toxic, misfolded proteins that initiate these diseases. One such protein, TDP-43, is implicated in multiple
Prevention and restoration of lactacystin-induced nigrostriatal dopamine neuron degeneration by novel brain-permeable iron chelators.
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Dysfunction of the ubiquitin-proteasome system (UPS) and accumulation of iron in substantia nigra (SN) are implicated in the pathogenesis of Parkinson's disease (PD). UPS dysfunction and iron misregulation may reinforce each other's contribution to the degeneration of dopamine (DA) neurons. In the
The subacute neurotoxicity of excess pyridoxine HCl and clioquinol (5-chloro-7-iodo-8-hydroxyquinoline) in beagle dogs. II. Pathology.
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The lesions caused by excess oral pyridoxine hydrochloride (150 mg/kg body weight/day) and clioquinol (200 mg/kg body weight/day), given individually and in combination to adult Beagle dogs, were evaluated. The experimental period was 100 to 112 days, except that four dogs in each of the clioquinol
PBT2 Reduces Toxicity in a C. elegans Model of polyQ Aggregation and Extends Lifespan, Reduces Striatal Atrophy and Improves Motor Performance in the R6/2 Mouse Model of Huntington's Disease.
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BACKGROUND
There is evidence that interaction with biologically important metals, particularly copper and iron, contributes to the pathological aggregation and toxicity of the mutant huntingtin protein in HD. PBT2 is a novel 8-hydroxyquinoline drug in clinical trials for AD and HD which restores
Vacuum-deposited, nonpolymeric flexible organic light-emitting devices.
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We demonstrate mechanically flexible, organic light-emitting devices (OLED's) based on the nonpolymetric thin-film materials tris-(8-hydroxyquinoline) aluminum (Alq(3)) and N, N(?) -diphenyl- N, N(?) -bis(3-methylphenyl)1- 1(?) biphenyl-4, 4(?) diamine (TPD). The single heterostructure is vacuum
Novel bifunctional drugs targeting monoamine oxidase inhibition and iron chelation as an approach to neuroprotection in Parkinson's disease and other neurodegenerative diseases.
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Iron has been shown to accumulates at site where neurons degenerate in neurodegenerative diseases of Parkinson's disease, Alzheimer's disease, Huntington disease, amyotrophic lateral sclerosis and Friedreich ataxia. Iron is thought to participate or initiate oxidative stress via generation of
Coordination properties of a metal chelator clioquinol to Zn(2+) studied by static DFT and ab initio molecular dynamics.
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Several lines of evidence supporting the role of metal ions in amyloid aggregation, one of the hallmarks of Alzheimer's disease (AD), have turned metal ion chelation into a promising therapeutic treatment. The design of efficient chelating ligands requires proper knowledge of the electronic and
Enhancement of third-order nonlinear optical susceptibility of Alq3 in polar aprotic solvents.
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The influence of solvent polarity on nonlinear optical properties of tris-(8-hydroxyquinoline)-aluminum (Alq3) was investigated by the degenerate four-wave mixing method at the 532 nm. It was obtained that the effective values of the third-order nonlinear optical susceptibility (χeff⟨3⟩)
Mutual stimulation of beta-amyloid fibrillogenesis by clioquinol and divalent metals.
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As reported by some authors, clioquinol (CQ), a 8-hydroxyquinoline derivative, has produced very encouraging results in the treatment of Alzheimer's disease (AD). Its biological effects are most likely ascribed to complexation of specific metal ions, such as copper (II) and zinc (II), critically
Time to fatigue is increased in mouse muscle at 37 degrees C; the role of iron and reactive oxygen species.
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Studies exploring the rate of fatigue in isolated muscle at 37 degrees C have produced mixed results. In the present study, muscle fibre bundles from the mouse foot were used to study the effect of temperature on the rate of muscle fatigue. Provided iron was excluded from the solutions, time to
Clioquinol, a drug for Alzheimer's disease specifically interfering with brain metal metabolism: structural characterization of its zinc(II) and copper(II) complexes.
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Clioquinol, a 8-hydroxyquinoline derivative, is producing very encouraging results in the treatment of Alzheimer's disease (AD). Its biological effects are most likely ascribed to complexation of specific metal ions, such as copper(II) and zinc(II), critically associated with protein aggregation and
Neurorescue activity, APP regulation and amyloid-beta peptide reduction by novel multi-functional brain permeable iron- chelating- antioxidants, M-30 and green tea polyphenol, EGCG.
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Accumulation of iron at sites where neurons degenerate in Parkinson's disease (PD) and Alzheimer's disease (AD) is thought to have a major role in oxidative stress induced process of neurodegeneration. The novel non-toxic lipophilic brain- permeable iron chelators, VK-28 (5- [4- (2- hydroxyethyl)
Iron-Chelating Drugs Enhance Cone Photoreceptor Survival in a Mouse Model of Retinitis Pigmentosa.
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Retinitis pigmentosa (RP) is a group of hereditary retinal degeneration in which mutations commonly result in the initial phase of rod cell death followed by gradual cone cell death. The mechanisms by which the mutations lead to photoreceptor cell death in RP have not been clearly elucidated. There
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