superoxide dismutase/atrophy

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Mice With a Combined Deficiency of Superoxide Dismutase 1 (Sod1), DJ-1 (Park7), and Parkin (Prkn) Develop Spontaneous Retinal Degeneration With Aging.

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Chronic oxidative stress is an important mechanism of disease in aging disorders. We do not have a good model to recapitulate AMD and other retinal disorders in which chronic oxidative stress plays an important role. We hypothesized that mice with a combined deficiency in superoxide

Degeneration of NO-synthesizing cerebrocortical neurons in transgenic mice expressing mutated superoxide dismutase is not due to elevated nitric oxide levels.

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Nitric oxide (NO) synthase (NOS)-containing cerebrocortical neurons degenerate in patients with amyotrophic lateral sclerosis (ALS) and dementia, and in transgenic mice expressing a mutated superoxide dismutase gene (G93A) associated with familial ALS. The cerebral cortex of transgenic mice

Familial amyotrophic lateral sclerosis with a two base pair deletion in superoxide dismutase 1: gene multisystem degeneration with intracytoplasmic hyaline inclusions in astrocytes.

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We performed a comparative neuropathological study on two siblings with familial amyotrophic lateral sclerosis (FALS). The clinical course of the sister who died at age 46 was 18 months, and that of the brother who died at age 65, 11 years. The neuropathological findings of the female were

Motoneuron degeneration after facial nerve avulsion is exacerbated in presymptomatic transgenic rats expressing human mutant Cu/Zn superoxide dismutase.

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We investigated motoneuron degeneration after proximal nerve injury in presymptomatic transgenic (tg) rats expressing human mutant Cu/Zn superoxide dismutase (SOD1). The right facial nerves of presymptomatic tg rats expressing human H46R or G93A SOD1 and their non-tg littermates were avulsed, and

Magnetic resonance imaging reveals neuronal degeneration in the brainstem of the superoxide dismutase 1 transgenic mouse model of amyotrophic lateral sclerosis.

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Magnetic resonance imaging (MRI) is becoming the preferred neuroimaging modality for the diagnosis of human amyotrophic lateral sclerosis (ALS). A useful animal model of ALS is the superoxide dismutase 1G93A G1H transgenic mouse, which shows many of the clinico-pathological features of the human

Immunodetection of disease-associated conformers of mutant cu/zn superoxide dismutase 1 selectively expressed in degenerating neurons in amyotrophic lateral sclerosis.

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We previously showed that some antipurinergic receptor P2X4 antibodies cross react with misfolded forms of amyotrophic lateral sclerosis (ALS)-linked mutant Cu/Zn superoxide dismutase (SOD1). Cross reactivity might be caused by abnormal exposure of an epitope in the inner hydrophobic region of SOD1

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

Mutant superoxide dismutase 1 (SOD1), a cause of amyotrophic lateral sclerosis, disrupts the recruitment of SMN, the spinal muscular atrophy protein to nuclear Cajal bodies.

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Spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS) are among the most common motor neuron diseases to afflict the human population. A deficiency of the survival of motor neuron (SMN) protein causes SMA and is also reported to be an exacerbating factor in the development of ALS.

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

Lipid peroxidation and superoxide dismutase activity in muscle and erythrocytes in adult muscular dystrophies and neurogenic atrophies.

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Lipid peroxidation (LP) and superoxide dismutase (SOD) activity were determined in erythrocytes and skeletal muscle obtained from patients with limb-girdle and facioscapulohumeral muscular dystrophies, neurogenic atrophies and from age-matched control subjects. Neither lipid peroxidation nor SOD

Amyotrophic lateral sclerosis associated with mutations in superoxide dismutase: a putative mechanism of degeneration.

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Amyotrophic lateral sclerosis (ALS) is a devastating neurologic disease that rapidly progresses from mild motor symptoms to severe motor paralysis and premature death. Until recently, there were few substantive studies conducted on the pathogenesis of the disease. With the genetic linkage of

TEMPOL, a superoxide dismutase mimic, ameliorates light-induced retinal degeneration.

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The efficacy of 4-hydroxy-2,2,6,6-tetramethylpiperidine-l-oxyl (TEMPOL), a metal independent superoxide dismutase (SOD) mimic, in ameliorating light-induced retinal degeneration was investigated. Thirty-six Lewis albino rats were exposed to green fluorescent light (490-580 nm, 160-180 foot-candles)

Transgenic murine dopaminergic neurons expressing human Cu/Zn superoxide dismutase exhibit increased density in culture, but no resistance to methylphenylpyridinium-induced degeneration.

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Primary dopaminergic neuronal cultures with increased superoxide dismutase (SOD) activity were established for studying the role of superoxide anion (O2-) in 1-methyl-4-phenylpyridinium (MPP+)-induced degeneration of dopamine (DA) neurons. Mean SOD activity in cultures prepared from transgenic

[Superoxide dismutase-1 (SOD-1) gene mutation-dependent mechanisms of neural degeneration in amyotrophic lateral sclerosis].

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease involving motor neuron degeneration, occurring in sporadic and familial forms. Mutations in Cu/Zn superoxide dismutase gene (SOD-1) play a key role in the pathogenesis of the familial form in which it is present in about 20%. The

Serum superoxide dismutase and malondialdehyde levels in a group of Chinese patients with age-related macular degeneration.

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OBJECTIVE The aim of this study was to investigate superoxide dismutase (SOD) activity together with malondialdehyde (MDA) levels in a group of Chinese patients with age-related macular degeneration (AMD). METHODS Serum SOD activity and MDA levels were analysed in 56 AMD patients with subtypes

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