Mitochondrial DNA Mutations in Aging, Disease and Cancer [Paperback]

Many human genetic diseases associated with blood, brain, colon, ear, eye, heart, kidney, liver, muscle, and pancreas are caused by mutations in mitochondrial DNA. Mutations in DNA can result in defects of the electron transport complexes, intermediates of the tricarboxylic acid cycle and substrate transport. The clinical manifestation of these diseases often involves muscle and the nervous system. Mitochondrial DNA mutations have now been associated with aging as well as age-related degenerative diseases such as Parkinson's, Alzheimer's, and Huntington's diseases. Changes in structure, function, and a number of mitochondria play an important role in carcinogenesis. Furthermore, the role of mitochondria in the execution of programmed cell death or apoptosis has been recognized recently.Many human genetic diseases associated with blood, brain, colon, ear, eye, heart, kidney, liver, muscle, and pancreas are caused by mutations in mitochondrial DNA. Mutations in DNA can result in defects of the electron transport complexes, intermediates of the tricarboxylic acid cycle and substrate transport. The clinical manifestation of these diseases often involves muscle and the nervous system. Mitochondrial DNA mutations have now been associated with aging as well as age-related degenerative diseases such as Parkinson's, Alzheimer's, and Huntington's diseases. Changes in structure, function, and a number of mitochondria play an important role in carcinogenesis. Furthermore, the role of mitochondria in the execution of programmed cell death or apoptosis has been recognized recently.Mitochondria in aging, disease, and cancer: an overview.- Mitochondria: structure, function and biogenesis.- The mitochondrial genetic system.- Mitochondrial gene inheritance and population genetics.- Mitochondrial DNA replication.- Genetic integrity of mitochondrial genome.- Modeling mitochondrial DNA mutations.- Mitochondrial control of apoptosis.- Differentiation between nuclear and mitochondrial-enclsB