α-Synuclein Promotes Mitochondrial Deficit and Oxidative Stress

By L. Hsu, Y. Sagara, A. Arroyo, E. Rockenstein, A. Sisk, M. Mallory, J. Wong, T. Takenouchi, M. Hashimoto, E. Masliah. 2000

649 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/0c5014f88eda6138b5ff4b2abc9eb2727067e20a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

In Neurology

In Physiology

Citations in the corpus

Dopamine-dependent neurotoxicity of α-synuclein: A mechanism for selective neurodegeneration in Parkinson disease (2002, background): “The molecular mechanisms underlying these pathological effects are unclear, although α-synuclein can induce oxidative stress and impair mitochondrial functio”
Parkinson-Like Neurodegeneration Induced by Targeted Overexpression of α-Synuclein in the Nigrostriatal System (2002, background): “Similarly, oxidative stress in combination with reduced levels of mitochondrial complex I and -synuclein aggregation have been proposed to underlie the selective death of nigral DA neurons in human PD (Hsu et al., 2000; Tabrizi et al., 2000).”
Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease (2019, background): “The mitochondrial accumulation of mutant (Martin et al., 2006) or wild‐ type (Hsu et al., 2000) α‐synuclein, the protein product of SNCA, in dopaminergic neurons reduces complex I activity and elevates ROS production in vivo in transgenic mice.”
α-Synuclein in Parkinson's disease. (2012, background): “…overexpression can induce ROS, and that suppressing these through molecular or pharmacological means may be neuroprotective in mammalian (Hsu et al. 2000; Clark et al. 2010; Liu et al. 2011) or insect systems (Wassef et al. 2007; Botella et al. 2008). a-SYNUCLEIN AT THE ER/GOLGI In a…”
Mechanism of Toxicity in Rotenone Models of Parkinson's Disease (2003, background): “On the other hand, elevated -synuclein expression can itself cause oxidative damage and render cells more vulnerable to oxidative insults (Hsu et al., 2000; Kanda et al., 2000; Ko et al., 2000).”
An In Vitro Model of Parkinson's Disease: Linking Mitochondrial Impairment to Altered α-Synuclein Metabolism and Oxidative Damage (2002, background): “Elevated -synuclein levels may cause oxidative stress (Hsu et al., 2000) as well as increased sensitivity to oxidative challenges (Kanda et al., 2000; Ko et al., 2000).”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “…of a -synuclein overexpression structural alterations of mitochondria, increased oxidative stress, and/or bioenergetic defects have been observed (Hsu et al , 2000; Martin et al , 2006; Stichel et al , 2007; Devi et al , 2008; Parihar et al , 2008; Liu et al , 2009; Chinta et al , 2010; Loeb et…”
The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “Structural and functional abnormalities of mitochondria have been observed with the overexpression of mutant or wild-type alpha-synuclein and have been associated with oxidative stress [263, 264].”
Unfolding the role of protein misfolding in neurodegenerative diseases (2003, background): “Finally, protein aggregates might induce OXIDATIVE STRESS by producing free radical species, resulting in protein and lipid oxidation, elevation of intracellular calcium and mitochondrial disfunctio”
Molecular pathophysiology of Parkinson's disease. (2005, background): “In addition to effects on the UPS, α-synuclein overexpression in cultured cells, particularly of mutant forms, has been linked to mitochondrial deficits (Hsu et al. 2000), defective cellular trafficking (Gosavi et al.”