Oxidative stress-induced posttranslational modifications of alpha-synuclein: Specific modification of alpha-synuclein by 4-hydroxy-2-nonenal increases dopaminergic toxicity

Xiang, Wei; Schlachetzki, J; Helling, Stefan; Bussmann, Julia; Berlinghof, Marvin; Schäffer, Tilman E.; Marcus, Katrin; Winkler, Jürgen; Klucken, Jochen; Becker, Cord‐Michael

doi:10.1016/j.mcn.2013.01.004

Cited by 141 publications

(124 citation statements)

References 45 publications

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“…Some studies have reported ageassociated increase in oxidative stress-led ROS as a contributor to formation of neuronal plaque, a-synuclein, and mHtt (Li et al, 2013), and other studies have suggested a role for amyloid b protein formation in ROS production (Behl et al, 1997;Abramov and Duchen, 2005;Shelat et al, 2008). Likewise with regard to PD pathology, it is reported that oxidative stress promotes a-synuclein aggregation in dopaminergic neurons, and that a-synuclein further generates intracellular ROS (Xiang et al, 2013). Furthermore, neuronal cell culture studies have implicated free radicals in misfolding and accumulation of mHttinduced neurotoxicity in PC12 cells.…”

Section: Oxidative Stress and Neurodegenerative Disordersmentioning

confidence: 99%

Oxidative Stress and the Central Nervous System

Salim

2016

J Pharmacol Exp Ther

903

518

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Section: Oxidative Stress and Neurodegenerative Disordersmentioning

confidence: 99%

Oxidative Stress and the Central Nervous System

Salim

2016

J Pharmacol Exp Ther

903

518

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“…Expression and toxicity of the small protein is increased under conditions of oxidative stress but is negatively regulated by the activity of heat shock proteins 216, 217, 218. Interestingly, α ‐synuclein has been reported to facilitate phosphorylation of tau by the above mentioned kinase GSK3 β 219…”

Section: Degenerative Pathomechanisms In Ibmmentioning

confidence: 99%

Immune and myodegenerative pathomechanisms in inclusion body myositis

Keller

Schmidt

Lünemann

2017

Ann Clin Transl Neurol

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Inclusion Body Myositis (IBM) is a relatively common acquired inflammatory myopathy in patients above 50 years of age. Pathological hallmarks of IBM are intramyofiber protein inclusions and endomysial inflammation, indicating that both myodegenerative and inflammatory mechanisms contribute to its pathogenesis. Impaired protein degradation by the autophagic machinery, which regulates innate and adaptive immune responses, in skeletal muscle fibers has recently been identified as a potential key pathomechanism in IBM. Immunotherapies, which are successfully used for treating other inflammatory myopathies lack efficacy in IBM and so far no effective treatment is available. Thus, a better understanding of the mechanistic pathways underlying progressive muscle weakness and atrophy in IBM is crucial in identifying novel promising targets for therapeutic intervention. Here, we discuss recent insights into the pathomechanistic network of mutually dependent inflammatory and degenerative events during IBM.

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“…α-synuclein is involved in neurotransmitter secretion as well as in the regulation of synaptic vesicle pool and plasticity [49][50][51] . By inducing lipid peroxidatin in the pathogenesis of Pakinson's disease it has been proposed that oxidative stress triggers a vicious cycle and accumulation of α-synuclein aggregates, which forms Lewy bodies, which are associated with neuronal dysfunction that triggers the onset of Parkinson's disease [52][53] . Inhibition of lipid peroxidation in neuronal cells could help to delay the ongoing neurodegeneration process in Parkinson's disease.…”

Section: Suppression Of Lipid Peroxidation In Parkinson's Diseasementioning

confidence: 99%

The Flavonoids Ameliorates: Protective Mechanisms in Neurodegenerative Diseases

Gupta¹,

Gupta²,

Gupta³

2017

Int. J. Curr. Res. Chem. Pharm. Sci

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Flavonids exhibits various neuroprotective actions. They have a potential to protect neurons against injury induced by neurot oxins in brain. Flavonoids also suppress neuro-inflammation and promote memory, learning and cognitive function. Oxidative stress is the well accepted concept in the etiology and progression of neurodegenerative diseases. Thus the therapeutic agent is targeted against suppressing and alleviating the oxidative stress-induced cellular damage. Flavonoids are reported to possess neuroprotective properties. In the present paper we reviewed the literature on the neuroprotective mechanism of flavonoids in protecting the dopaminergic neurons. Various mechanisms like flavonoids as a mitochondrial target therapy, effect of flavonoids in suppressing the lipid peroxidation, activation of intracellular antioxidant enzymes are reviewed.

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Oxidative stress-induced posttranslational modifications of alpha-synuclein: Specific modification of alpha-synuclein by 4-hydroxy-2-nonenal increases dopaminergic toxicity

Cited by 141 publications

References 45 publications

Oxidative Stress and the Central Nervous System

Oxidative Stress and the Central Nervous System

Immune and myodegenerative pathomechanisms in inclusion body myositis

The Flavonoids Ameliorates: Protective Mechanisms in Neurodegenerative Diseases

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