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Douglas Wallace, PhD, FACMG

Douglas Wallace is the UCI Donald Bren Professor of Biological Sciences and Molecular Medicine. Wallace is one of the world‘s leading geneticists, whose work ranges from tracing the origins of the human species to finding the causes of degenerative diseases, cancer and aging. A member of the National Academy of Sciences, Wallace in 1994 received the William Allan Award, the American Society of Human Genetics’ highest recognition for contributions to human genetics. He also has shared the Passano Award

2000 for mitochondrial genetics and received the 2000 Metropolitan Life Foundation Research Award for Medical Research in Alzheimer’s Disease. He is director of the UCI Center for Molecular and Mitochondrial Medicine and Genetics MAMMAG.
From the demonstration of the first human mitochondrial lesion in 1975 (chloramphenicol resistance) to the delineation of a mitochondrial mutation in 1990 as the basis of a type of myoclonic epilepsy, Wallace has almost single-handedly written a major chapter in human molecular genetics.
Research Interests: For the past twenty-five years, my colleagues and I have been studying the genetics of the human mitochondrion and the role of mitochondrial DNA (mtDNA) variation in human evolution and degenerataive diseases. In our early studies, we demonstrated that the human mtDNA could encode heritable traits, was maternally inherited, and had a high mutation rate. More recently, we have analyzed the continental distribution of common mtDNA polymorphisms and used this information to reconstruct the human family tree, trace the migration of women out of Africa and into various continents, and investigate the origins of Native Americans. Concurrently, we have demonstrated that deleterious mtDNA mutations are common and can cause a variety of degenerative diseases, including blindness, diabetes, epilepsy, movement disorders, and dementias. We are now exploring the possibility that the age-related accumulation of mtDNA mutations in tissues and organs may play an important role in aging and senescence.