Cell Death
ALS Diet Pages
"Our findings emphasize the importance of defense responses and cytoskeletal, mitochondrial and proteasomal dysfunction, reflect reduced neuronal maintenance and vesicle trafficking, and implicate impaired ion homeostasis and glycolysis in ALS pathogenesis. Contrary to expectations for a tissue under oxidative stress, nuclear-encoded mitochondrial genes are uniformly down-regulated. Moreover, the down-regulation of mitochondrial and glycolytic genes implies a combined reduction of mitochondrial and cytoplasmic energy supply, with a possible role in the death of ALS motoneurons. Lederer CW et al. Pathways and genes differentially expressed in the motor cortex of patients with sporadic amyotrophic lateral sclerosis. BMC Genomics. 2007 Jan 23;8:26.
"The results are consistent with previous data demonstrating that cytochrome oxidase, not iron-sulfur enzymes, is the primary target for NO inhibition of brain cell respiration" Brown, G.C., Nitric oxide and mitochondrial respiration. Biochim. Biophys. Acta., 1411, 351-369 (1999).
ALS Diet Pages

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Amyotrophic Lateral Sclerosis
Please click the PDF icon to the left to read or download the entire 36 page Amyotrophic Lateral Sclerosis Diet by Dr. David Steenblock
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