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- W1489780864 abstract "This chapter discusses the genetic basis and molecular pathogenesis of Huntington's disease (HD). The discovery of the HD gene on chromosome 4 in 1993 was a major step forward. The HD gene is expanded with an excess number of CAG trinucleotide repeats that result in a long stretch of polyglutamine in the expressed protein. Expansion of trinucleotide repeats is now recognized as a major cause of neurological disease. Recently it has been thought that HD may result from impaired mitochondrial oxidative phosphorylation because an identical pattern of differential neuronal loss can be produced in rodents and primates by mitochondrial electron transport chain inhibitors. These inhibitors cause partial energy failure that triggers N-methyl-D-aspartate-receptor mediated excitotoxic injury, decreased free radical scavenging, and increased production of free radicals. Other indirect lines of evidence suggest a possible role for mitochondrial abnormalities in the pathogenesis of HD as well. Other indirect lines of evidence suggest a possible role for mitochondria in the pathogenesis of HD." @default.
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- W1489780864 date "1999-01-01" @default.
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- W1489780864 title "Chapter 3 The Genetic Basis and Molecular Pathogenesis of Huntington's Disease" @default.
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- W1489780864 doi "https://doi.org/10.1016/s1566-3124(08)60023-1" @default.
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