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Current perspectives in the treatment of mitochondrial DNA diseases.

Defects of the mitochondrial genome are an important cause of genetic disease (1). The clinical features are very varied but in many individuals the defect leads to progressive problems which may result in severe disability and even death. It is against the background of increasing recognition and detection of mitochondrial DNA (mtDNA) disorders that clinicians and scientists must strive to develop effective therapies. In this article we discuss agents that are currently being used in patients (largely unsuccessfully) and possible future therapies. One of the major difficulties when assessing a potential therapy for mtDNA disorders is the clinical variability of the disease. Thus patients with the same genetic defect may present in a variety of different ways and the disease may take an entirely different course. This means that clinical trials are difficult to perform. In addition, we know relatively little about the natural history of these disorders and collecting enough patients with a similar phenotype in one centre is very difficult. Many drugs used in the treatment of mitochondrial disease therefore only have anecdotal data rather than clinical trials to support their use. All mitochondrial disorders result from the progressive decline in the ability to supply cellular energy demands in the form of available AT P. The respiratory chain is also a potent source of free radicals, thus a respiratory chain defect can result in ATP deficiency and an excess production of free radicals. Biochemical strategies have sought to increase the production