S
Sandra L. Siedlak
Researcher at Case Western Reserve University
Publications - 158
Citations - 12537
Sandra L. Siedlak is an academic researcher from Case Western Reserve University. The author has contributed to research in topics: Alzheimer's disease & Oxidative stress. The author has an hindex of 57, co-authored 155 publications receiving 11408 citations. Previous affiliations of Sandra L. Siedlak include Autonomous University of Madrid & Asahikawa Medical University.
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Journal ArticleDOI
Mitochondrial abnormalities in Alzheimer's disease.
Keisuke Hirai,Gjumrakch Aliev,Akihiko Nunomura,Akihiko Nunomura,Hisashi Fujioka,Robert L. Russell,Craig S. Atwood,Anne B. Johnson,Yvonne Kress,Harry V. Vinters,Massimo Tabaton,Shun Shimohama,Adam D. Cash,Sandra L. Siedlak,Peggy L.R. Harris,Paul K. Jones,Robert B. Petersen,George Perry,Mark A. Smith +18 more
TL;DR: Morphometric analysis showed that mitochondria are significantly reduced in Alzheimer's disease, and the relationship shown here between the site and extent of mitochondrial abnormalities and oxidative damage suggests an intimate and early association between these features in dementia.
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Amyloid-β overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins
Xinglong Wang,Bo Su,Sandra L. Siedlak,Paula I. Moreira,Hisashi Fujioka,Yang Wang,Gemma Casadesus,Xiongwei Zhu +7 more
TL;DR: APP, through amyloid β production, causes an imbalance of mitochondrial fission/fusion that results in mitochondrial fragmentation and abnormal distribution, which contributes to mitochondrial and neuronal dysfunction.
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Metal Binding and Oxidation of Amyloid-β within Isolated Senile Plaque Cores: Raman Microscopic Evidence†
Jian Dong,Craig S. Atwood,Vernon E. Anderson,Sandra L. Siedlak,Mark A. Smith,George Perry,Paul R. Carey +6 more
TL;DR: The results indicate that Abeta in vivo is a metalloprotein, and the loosening of the structure following chelation treatment suggests a possible means for the solubilization of amyloid deposits.
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Amyloid‐β Deposition in Alzheimer Transgenic Mice Is Associated with Oxidative Stress
Mark A. Smith,Keisuke Hirai,Karen Hsiao,Miguel A. Pappolla,Peggy L.R. Harris,Sandra L. Siedlak,Massimo Tabaton,George Perry +7 more
TL;DR: Evidence that amyloid‐β and oxidative damage are inextricably linked in vivo is provided, and the use of transgenic animals for the development of antioxidant therapeutic strategies is supported.
Journal ArticleDOI
Increased Iron and Free Radical Generation in Preclinical Alzheimer Disease and Mild Cognitive Impairment
Mark A. Smith,Xiongwei Zhu,Massimo Tabaton,Gang Liu,Daniel W. McKeel,Mark L. Cohen,Xinglong Wang,Sandra L. Siedlak,Barney E. Dwyer,Barney E. Dwyer,Takaaki Hayashi,Masao Nakamura,Akihiko Nunomura,George Perry,George Perry +14 more
TL;DR: It is found that an imbalance in iron homeostasis is a precursor to the neurodegenerative processes leading to AD and that iron imbalance is not necessarily unique to affected regions, and an understanding of iron deposition in other regions of the brain may provide insights into neuroprotective strategies.