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In recent years, the question of whether mitochondrial dysfunction can play a role in neurodegenerative diseases has been the focus of considerable attention. A series of studies point to an inverse relationship between mitochondrial complex I and II activities and neurodegenerative disorders including Alzheimer's disease and Parkinson's disease. Here, we use the computer simulation analysis of the standard model of central respiratory chain disorders to quantitatively estimate the contribution of mitochondrial malfunction to neurodegeneration. Mitochondrial energy metabolism is implicated in the pathogenesis of most neurodegenerative diseases including Alzheimer's, Huntington's, and Parkinson's diseases, as well as certain polyglutamine diseases and amyotrophic lateral sclerosis. This model is based on recent data demonstrating a quantitative relationship between the extent of respiratory chain dysfunction and the ability of cells to resist apoptosis. We used an underlying biochemical model to quantitatively estimate the extent to which mitochondrial malfunction can contribute to the neurodegenerative process. In general, mitochondrial dysfunction is a secondary phenomenon as the cell attempts to regulate ATP levels. Furthermore, it is important to emphasize that most of the neurodegenerative diseases, including those studied, are not homogeneous. For example, Alzheimer's disease has a mixed phenotype that includes patients with both familial and sporadic forms. Another important factor in the contribution of mitochondria to neurodegenerative disorders is the extent of energy demand in a given area of the brain.Q:
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