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Abbyann Sisk
Researcher at University of California, San Diego
Publications - 6
Citations - 3706
Abbyann Sisk is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Alpha-synuclein & Beta-synuclein. The author has an hindex of 6, co-authored 6 publications receiving 3558 citations.
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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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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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Oxidative stress induces amyloid-like aggregate formation of NACP/alpha-synuclein in vitro.
TL;DR: It is suggested that NACP/alpha-synuclein aggregation might be closely related to oxidative reactions which may play a critical role in neurodegeneration in disorders with Lewy bodies.
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Comparison of Neurodegenerative Pathology in Transgenic Mice Overexpressing V717F β-Amyloid Precursor Protein and Alzheimer’s Disease
TL;DR: These findings show that overproduction of hAPP717V→F in tg mice is sufficient to cause not only amyloid deposition, but also many of the complex subcellular degenerative changes associated with AD.
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Enhanced substantia nigra mitochondrial pathology in human alpha-synuclein transgenic mice after treatment with MPTP.
David D. Song,Clifford W. Shults,Clifford W. Shults,Abbyann Sisk,Edward Rockenstein,Eliezer Masliah +5 more
TL;DR: In this article, α-synuclein (α-S) was shown to enhance substantia nigra (SN) pathology resulting from treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).