D
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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Bioenergetics in human evolution and disease: implications for the origins of biological complexity and the missing genetic variation of common diseases.
TL;DR: The neutralist–selectionist debate is a consequence of mammals having two different evolutionary strategies: a fast mtDNA strategy for intra-specific radiation and a slow n DNA strategy for speciation, both of which have been missed by large, inter-population association studies.
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Leber's hereditary optic neuropathy plus dystonia is caused by a mitochondrial DNA point mutation
John M. Shoffner,Michael D. Brown,Carol Stugard,Albert S. June,Stephen C. Pollock,Richard H. Haas,Allan Kaufman,Deborah A. Koontz,Yoon L. Kim,Jennifer R. Graham,Edwin R. Smith,John Dixon,Douglas C. Wallace +12 more
TL;DR: A point mutation in the ND6 subunit of complex I at position 14,459 of the mitochondrial DNA (MTND6*LDY T 14459A) was identified as a candidate mutation for the highly tissue-specific disease.
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The age-related accumulation of a mitochondrial DNA control region mutation in muscle, but not brain, detected by a sensitive PNA-directed PCR clamping based method
TL;DR: The peptide nucleic acid (PNA)-directed PCR clamping technique was modified and applied to the detection of mitochondrial DNA mutations with low heteroplasmy, demonstrating that the 3243 and 8344 mutations do not accumulate with age to levels greater than 0.1% in brain and muscle.
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Mitochondrial biology, degenerative diseases and aging
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Marked increase in mitochondrial DNA deletion levels in the cerebral cortex of Huntington's disease patients
Terzah M. Horton,Brett H. Graham,Marisol Corral-Debrinski,John M. Shoffner,Allan Kaufman,M F Beal,Douglas C. Wallace +6 more
TL;DR: The hypothesis that HD is associated with elevated cortical mtDNA damage is supported by the quantitated amount of the common mitochondrial 4977 nucleotide pair deletion in cortex and putamen of HD patients and age-matched controls by the serial dilution-polymerase chain reaction method.