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Nicotinamide adenine dinucleotide prevents neuroaxonal degeneration induced by manganese in cochlear organotypic cultures.
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Manganese (Mn) is an essential trace mineral for normal growth and development. Persistent exposures to high atmospheric levels of Mn have deleterious effects on CNS and peripheral nerves including those associated with the auditory system. Nicotinamide adenine dinucleotide (NAD) is a coenzyme which
Recombinant Manganese Peroxidase Reduces A2E Burden in Age-Related and Stargardt's Macular Degeneration Models.
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Macular degeneration is hallmarked by retinal accumulation of toxic retinoid species (e.g., A2E) for which there is no endogenous mechanism to eliminate it. This ultimately results in progressive dysfunction and loss of vision either in advanced age for genetically normal patients (age-related
[Chronic acquired hepatocerebral degeneration: the role of manganese and treatment by endovascular occlusion of a porto-systemic shunt].
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This case report describes a 74 year-old woman with cirrhosis who developed choreo-athetotic movements associated with elevated whole blood manganese and symmetric hyperintense pallidum on T1-weighted magnetic resonance imaging. The diagnosis was chronic acquired hepatocerebral degeneration. The
Manganese-induced neurotoxicity: the role of astroglial-derived nitric oxide in striatal interneuron degeneration.
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Chronic exposure to excessive manganese (Mn) is the cause of a neurodegenerative movement disorder, termed manganism, resulting from degeneration of neurons within the basal ganglia. Pathogenic mechanisms underlying this disorder are not fully understood but involve inflammatory activation of glial
Genetic association of manganese superoxide dismutase with exudative age-related macular degeneration.
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OBJECTIVE
To elucidate whether any polymorphic genes for xenobiotic-metabolizing and antioxidant enzymes are associated with the development of exudative age-related macular degeneration.
METHODS
A hospital-based case-control study was performed on a consecutive series of 102 Japanese patients with
Manganese-Enhanced MRI for Preclinical Evaluation of Retinal Degeneration Treatments.
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OBJECTIVE
Apply manganese-enhanced magnetic resonance imaging (MEMRI) to assess ion channel activity and structure of retinas from mice subject to light-induced retinal degeneration treated with prophylactic agents.
METHODS
Abca4(-/-)Rdh8(-/-) double knockout mice with and without prophylactic
Manganese superoxide dismutase (MnSOD) gene (Ala-9Val, Ile58Thr) polymorphism in patients with age-related macular degeneration (AMD).
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BACKGROUND
Oxidative stress is involved in the pathogenesis of many chronic disorders including cancer, inflammation, and neurologic diseases. Reactive oxygen species (ROS) may play a major role in age-related macular degeneration (AMD). This study investigated the mRNA and protein profiles of
Spermine protects alpha-synuclein expressing dopaminergic neurons from manganese-induced degeneration.
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Manganese exposure is among the many environmental risk factors linked to the progression of neurodegenerative diseases, such as manganese-induced parkinsonism. In animal models, chronic exposure to manganese causes loss of cell viability, neurodegeneration, and functional deficits. Polyamines, such
Implications of Manganese in Chronic Acquired Hepatocerebral Degeneration.
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Neurological symptoms can be one of the over-riding symptoms in patients with liver cirrhosis. Patients can present with subtle changes in mood or neurological function due to hepatic encephalopathy (HE), to more severe presentations including stupor and coma. While HE, in its severe form, can be
Chronic acquired hepatocerebral degeneration, pallidal T1 MRI hyperintensity and manganese in a series of cirrhotic patients.
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Chronic acquired hepatocerebral degeneration (CAHD) is a rare neurological disorder of cirrhotic patients, characterized by parkinsonism and cognitive impairment. A T1 hyperintensity on the globus pallidum due to an accumulation of manganese (Mn) is found in these patients. The aim of the study was
Autosomal-Recessive Intellectual Disability with Cerebellar Atrophy Syndrome Caused by Mutation of the Manganese and Zinc Transporter Gene SLC39A8.
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Manganese (Mn) and zinc (Zn) are essential divalent cations used by cells as protein cofactors; various human studies and animal models have demonstrated the importance of Mn and Zn for development. Here we describe an autosomal-recessive disorder in six individuals from the Hutterite community and
Inconsistency between manganese superoxide dismutase expression and its activity involved in the degeneration of recognition function induced by chronic aluminum overloading in mice.
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Manganese (Mn) superoxide dismutase (SOD) is mainly located in mitochondrial matrix and is responsible for scavenging about 80% free radicals from oxidative and phospharylative process in mitochondria. It was reported that the insufficiency of Mn SOD expression or activity was connected to the
Effect of trientine on manganese intoxication in a patient with acquired hepatocerebral degeneration.
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[Hyperkinetic dystonic syndrome due to manganese poisoning with mental degeneration; clinical observation].
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Levodopa, manganese, and degenerations of the brain.
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