LMP410H1 Lecture Notes - Lecture 6: Huntingtin, Glutamine, Neuroglia
31 Mar 2016
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Lecture 6 trinucleotide repeat diseases & huntington"s. Repeats of cag which when transcribed becomes polyglutamine stretches these are usually really small but become larger in size and you usually get disease. Anicipaion means there is a variaion in repeat lengths and it tends to get longer but it can get shorter too. If your child is born with 36 or more, you can never decrease in lengths of cag repeats : neurons lost are usually the pyramidal and spiny neurons in the striatum. Because the huningin protein aggregates in both the nucleus and the cytoplasm and in both these cases, when you look at the high magniicaion, you can see ibers similar to ad and pd . Pathogenicity of huningin protein (ht) mutants does not afect mrna : intercellular. Present in both neurons as well as astrocytes and microglial cells (immune cells) Remember they cause the inlammatory porion of the disease .
