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Siegel GJ, Agranoff BW, Albers RW, et al., editors. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition. Philadelphia: Lippincott-Raven; 1999.

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Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition.

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Nutrition and the Treatment of Neurodegenerative Disease

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An understanding of the interaction of brain and nutrition permits the use of diet to treat neurological disorders. One of the best-known examples is phenylketonuria. This disease results from the near absence of phenylalanine hydroxylase, an enzyme which converts phenylalanine to tyrosine. This deficit results in excessive phenylalanine in the blood and severe mental retardation. Dietary control of phenylalanine largely protects the brain from this otherwise devastating condition (see Chap. 44). Diet can also be used to bypass inborn errors in oxidative metabolism (see Chap. 44). The neurological status of patients with diminished pyruvate dehydrogenase activity can be improved with a diet that is high in ketones, which bypasses the pyruvate dehydrogenase step in brain metabolism. A diet enriched in antioxidants may be particularly useful in treating neurodegenerative disorders. Treatment with vitamin E of patients with moderately severe impairment from Alzheimer's disease has been reported to slow the progression of disease [36]. Nutritional approaches to ameliorate age-related changes in the brain are discussed above.

The concentration of Zn2+ is altered in many disorders of the CNS. For example, chronic alcoholism is associated with low serum Zn2+. Low brain Zn2+ may enhance NMDA excitotoxicity and ethanol-withdrawal seizure susceptibility. Also, Zn2+ deficiency can produce neuronal damage through increased free radical formation. Zn2+ replacement therapy may be a rational approach to the treatment of alcohol-withdrawal seizures and alcohol-related brain dysfunction. Other diseases said to be associated with low serum Zn2+ include Alzheimer-type dementia, amyotrophic lateral sclerosis, Down's syndrome, epilepsy, Friedreich's ataxia, Guillain-Barré syndrome, hepatic encephalopathy, multiple sclerosis, Parkinson's disease, Pick's disease, retinitis pigmentosa, retinal dystrophy, schizophrenia and Wernicke-Korsakoff syndrome. The status of metallothionein isoforms and other low-molecular-weight, Zn2+-binding proteins in these conditions is unknown. Several of these disorders are associated with oxidative stress: since metallothioneins are able to prevent the formation of free radicals, induction of metallothioneins may provide long-lasting protection against oxidative damage [37].

By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed.

Copyright © 1999, American Society for Neurochemistry.
Bookshelf ID: NBK28166

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