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Douglas C. Wallace
Researcher at Children's Hospital of Philadelphia
Publications - 495
Citations - 77420
Douglas C. Wallace is an academic researcher from Children's Hospital of Philadelphia. The author has contributed to research in topics: Mitochondrial DNA & Mitochondrion. The author has an hindex of 134, co-authored 475 publications receiving 72035 citations. Previous affiliations of Douglas C. Wallace include University of California & Stanford University.
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Journal ArticleDOI
mtDNA Haplogroup X: An Ancient Link between Europe/Western Asia and North America?
Michael D. Brown,Seyed H. Hosseini,Antonio Torroni,Hans-Jürgen Bandelt,Jon C. Allen,Theodore G. Schurr,Rosaria Scozzari,Fulvio Cruciani,Douglas C. Wallace +8 more
TL;DR: Time estimates for the arrival of X in North America are 12,000-36,000 years ago, thus supporting the conclusion that the peoples harboring haplogroup X were among the original founders of Native American populations.
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Mitochondrial Function, Biology, and Role in Disease A Scientific Statement From the American Heart Association
Elizabeth Murphy,Hossein Ardehali,Robert S. Balaban,Fabio DiLisa,Gerald W. Dorn,Richard N. Kitsis,Kinya Otsu,Peipei Ping,Rosario Rizzuto,Michael N. Sack,Douglas C. Wallace,Richard J. Youle +11 more
TL;DR: This statement will define the key roles that mitochondria play in cardiovascular physiology and disease and provide insight into how mitochondrial defects can contribute to cardiovascular disease; it will also discuss potential biomarkers of mitochondrial disease and suggest potential novel therapeutic approaches.
Journal ArticleDOI
Lifespan Extension and Rescue of Spongiform Encephalopathy in Superoxide Dismutase 2 Nullizygous Mice Treated with Superoxide Dismutase–Catalase Mimetics
Simon Melov,Susan R. Doctrow,Julie A. Schneider,Joanna Haberson,Manisha Patel,Pinar Coskun,Karl Huffman,Douglas C. Wallace,Bernard Malfroy +8 more
TL;DR: It is shown that treatment of sod2 nullizygous mice with synthetic superoxide dismutase (SOD)–catalase mimetics extends their lifespan by threefold, rescues the spongiform encephalopathy, and attenuates mitochondrial defects.
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Marked changes in mitochondrial DNA deletion levels in Alzheimer brains
Marisol Corral-Debrinski,Terzah M. Horton,M. T. Lott,John M. Shoffner,Ann C. McKee,M F Beal,Brett H. Graham,Douglas C. Wallace +7 more
TL;DR: The hypothesis that OXPHOS defects resulting from somatic mtDNA mutations may play a role in AD pathophysiology is supported.
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Mitochondria and cancer: Warburg addressed.
TL;DR: It now appears that cancer cells generate excessive lactate in the presence of oxygen is the product of two factors: a return to the more glycolytic metabolism of the embryo and alterations in oxidative phosphorylation to increase mitochondrial reactive oxygen species (ROS) production.