Effects of Enhanced Striatal Dopamine Turnover In Vivo on Glutathione Oxidation

Loeffler, David A.; DeMaggio, A. J.; Juneau, Paul; Havaich, M.; LeWitt, P. A.

doi:10.1097/00002826-199408000-00009

Cited by 58 publications

(43 citation statements)

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“…The importance of this finding is reflected by the fact that DA neurons possess reduced antioxidant capacity, as evidenced by low intracellular glutathione (40). Thus, DA neurons are inherently more vulnerable to oxidative stress and microglia activation, when compared with other cell types (40). To our knowledge, this is the first report using PHOX Ϫ/Ϫ mutants that clearly shows the role of NADPH oxidase-generated superoxide in LPS-induced dopaminergic toxicity.…”

Section: Discussionmentioning

confidence: 96%

“…These observations strongly indicate that activation of NADPH oxidase and the subsequent release of superoxide are critical for LPS-induced neurotoxicity. The importance of this finding is reflected by the fact that DA neurons possess reduced antioxidant capacity, as evidenced by low intracellular glutathione (40). Thus, DA neurons are inherently more vulnerable to oxidative stress and microglia activation, when compared with other cell types (40).…”

Section: Discussionmentioning

confidence: 99%

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NADPH Oxidase Mediates Lipopolysaccharide-induced Neurotoxicity and Proinflammatory Gene Expression in Activated Microglia

Qin

Liu

Wang

et al. 2004

Journal of Biological Chemistry

539

492

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Parkinson's disease is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra. We have previously reported that lipopolysaccharide (LPS)-induced degeneration of dopaminergic neurons is mediated by the release of proinflammatory factors from activated microglia. Here, we report the pivotal role of NADPH oxidase in inflammation-mediated neurotoxicity, where the LPS-induced loss of nigral dopaminergic neurons in vivo was significantly less pronounced in NADPH oxidase-deficient (PHOX

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

NADPH Oxidase Mediates Lipopolysaccharide-induced Neurotoxicity and Proinflammatory Gene Expression in Activated Microglia

Qin

Liu

Wang

et al. 2004

Journal of Biological Chemistry

539

492

View full text Add to dashboard Cite

show abstract

“…It has been suggested that the increased turnover of DA and dopaminergic neurodegeneration are associated with oxidative stress derived from an increased production of hydrogen peroxide, which is formed during the oxidative deamination of DA by MAO (29,31). A recent study showed that activated MAO induces α-synuclein aggregation, which may be associated with early Parkinsonism and dopaminergic neurodegeneration in the substantia nigra in SMAD family member 3-null mice (32).…”

Section: Involvement Of Mao In Neurodegenerationmentioning

confidence: 99%

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Cai

2014

Molecular Medicine Reports

180

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Abstract. Activated monoamine oxidase (MAO) has a critical role in the pathogenesis of Alzheimer's disease (AD), including the formation of amyloid plaques from amyloid β peptide (Aβ) production and accumulation, formation of neurofibrillary tangles, and cognitive impairment via the destruction of cholinergic neurons and disorder of the cholinergic system. Several studies have indicated that MAO inhibitors improve cognitive deficits and reverse Aβ pathology by modulating proteolytic cleavage of amyloid precursor protein and decreasing Aβ protein fragments. Thus, MAO inhibitors may be considered as promising therapeutic agents for AD.

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“…The selective loss of DA neurons is likely due to the increased vulnerability of these cells to oxidative stress, as these neurons have lower levels of glutathione compared with other cell types, and are thus more responsive to the effects of mitochondrial dysfunction ( [96,142]). In addition to oxidative stress also other mechanisms have been proposed to be involved in selective DA neuron degeneration in PD, including excitotoxicity, intracellular calcium and metal ion rise, neurofibrillary tangle formation and disruption of the cytoskeletal transport [112].…”

Section: Parkinson's Disease and Neuroinflammationmentioning

confidence: 99%

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

Vegeto

Benedusi

Maggi

2008

Frontiers in Neuroendocrinology

278

206

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a b s t r a c tRecent studies highlight the prominent role played by estrogens in protecting the central nervous system (CNS) against the noxious consequences of a chronic inflammatory reaction. The neurodegenerative process of several CNS diseases, including Multiple Sclerosis, Alzheimer's and Parkinson's Diseases, is associated with the activation of microglia cells, which drive the resident inflammatory response. Chronically stimulated during neurodegeneration, microglia cells are thought to provide detrimental effects on surrounding neurons. The inhibitory activity of estrogens on neuroinflammation and specifically on microglia might thus be considered as a beneficial therapeutic opportunity for delaying the onset or progression of neurodegenerative diseases; in addition, understanding the peculiar activity of this female hormone on inflammatory signalling pathways will possibly lead to the development of selected anti-inflammatory molecules. This review summarises the evidence for the involvement of microglia in neuroinflammation and the anti-inflammatory activity played by estrogens specifically in microglia.

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Effects of Enhanced Striatal Dopamine Turnover In Vivo on Glutathione Oxidation

Cited by 58 publications

References 0 publications

NADPH Oxidase Mediates Lipopolysaccharide-induced Neurotoxicity and Proinflammatory Gene Expression in Activated Microglia

NADPH Oxidase Mediates Lipopolysaccharide-induced Neurotoxicity and Proinflammatory Gene Expression in Activated Microglia

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

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