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Yutaka Sagara
Researcher at Salk Institute for Biological Studies
Publications - 24
Citations - 6491
Yutaka Sagara is an academic researcher from Salk Institute for Biological Studies. The author has contributed to research in topics: Oxidative stress & Reactive oxygen species. The author has an hindex of 20, co-authored 24 publications receiving 6231 citations. Previous affiliations of Yutaka Sagara include University of California, San Diego.
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Journal ArticleDOI
Dopaminergic Loss and Inclusion Body Formation in α-Synuclein Mice: Implications for Neurodegenerative Disorders
Eliezer Masliah,Edward Rockenstein,Isaac Veinbergs,Margaret Mallory,Makoto Hashimoto,Ayako Takeda,Yutaka Sagara,Abbyann Sisk,Lennart Mucke +8 more
TL;DR: Results suggest that accumulation of wild-type alpha-synuclein may play a causal role in Parkinson's disease and related conditions.
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Flavonoids protect neuronal cells from oxidative stress by three distinct mechanisms.
TL;DR: Three structural requirements of flavonoids for protection from glutamate are the hydroxylated C3, an unsaturated C ring, and hydrophobicity, and three distinct mechanisms of protection are found, which show that the mechanism of protection from oxidative insults by flavonoid is highly specific for each compound.
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The Regulation of Reactive Oxygen Species Production during Programmed Cell Death
TL;DR: It is found that GSH depletion is not sufficient to cause the maximal mitochondrial ROS production, and that there is an early requirement for protease activation, changes in gene expression, and a late requirement for Ca2+ mobilization.
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α-Synuclein Promotes Mitochondrial Deficit and Oxidative Stress
Leigh J. Hsu,Yutaka Sagara,Armando Arroyo,Edward Rockenstein,Abbyann Sisk,Margaret Mallory,Jeffrey J. Wong,Takato Takenouchi,Makoto Hashimoto,Eliezer Masliah +9 more
TL;DR: Results suggest that abnormal accumulation of α-synuclein could lead to mitochondrial alterations that may result in oxidative stress and, eventually, cell death.
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β-Amyloid peptides enhance α-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease
Eliezer Masliah,Edward Rockenstein,Isaac Veinbergs,Yutaka Sagara,Margaret Mallory,Makoto Hashimoto,Lennart Mucke +6 more
TL;DR: Treatments that block the production or accumulation of β-amyloid peptides could benefit a broader spectrum of disorders than previously anticipated.