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A Mitochondrial Etiology of Metabolic and Degenerative Diseases, Cancer and Aging
NIH VideoCast
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65K views12 years ago
Aging and longevityHeart and metabolismBiology of agingMetabolism and energyCancer biology
How mitochondrial genetics and energy production play a central role in metabolic diseases, cancer, and aging.
A Mitochondrial Etiology of Metabolic and Degenerative Diseases, Cancer and Aging Air date: Wednesday, April 02, 2014, PM Category: Wednesday Afternoon Lectures Runtime: Description: Wednesday Afternoon Lecture Series For half a millennium Western medicine has focused on anatomy and for the past century on nuclear DNA (nDNA), Mendelian, genetics. While these concepts have permitted many biomedical advances, they have proven insufficient for understanding the common "complex" diseases. Life requires energy, 90 percent of which comes from the mitochondrion. The mitochondrial genome consists of thousands of copies of the maternally inherited mitochondrial DNA (mtDNA) plus 1,000--2,000 nDNA genes. The mtDNA has a very high mutation rate, but the most deleterious mutations are removed by an ovarian prefertilization selection system. Hence, functional mtDNA variants are constantly being introduced into the human population, the more deleterious resulting in recent maternally inherited diseases. The milder mtDNA variants have accumulated sequentially as women spread throughout Africa and migrated out to colonize Eurasia and the Americas. Some ancient mtDNA variants alter mitochondrial energy metabolism in ways that were beneficial in different regional environments. In alternative environments and/or with age these same adaptive variants can be maladaptive and increase the risk for disease. For example, one variant increases the penetrance of mutations associated with an inherited form of vision loss, but is adaptive for survival at high altitudes. Mutations in the mtDNAs also accumulate with age in both stem and somatic tissue cells and can be associated with various forms of cancer. The introduction of mtDNA variants into the mouse germline via female embryonic stem cells has confirmed the causal role of mitochondrial deficiency in diseases. Hence, the pathophysiology of some common diseases may be bioenergetic dysfunction and their genetic complexity the result of thousands of nDNA and mtDNA bioenergetic gene variants interacting. For more information go to wals.od.nih.gov Author: Douglas Wallace, Perelman School of Medicine at the University of Pennsylvania Permanent link: videocast.nih.gov/launch.asp?18367Why it's here
From a health institutionNIH VideoCast is on Rounds' list of health institutions, and this upload is one of its most-watched lectures or explainers. Nobody has recommended it in the communities yet, so it ranks below community picks.