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Although each model differs in terms of CAG repeat length and transgene expression levels, and thus in the severity of the resulting HD phenotype, they were instrumental in demonstrating a fundamental feature of the disease, namely that severe neuronal dysfunction precedes degeneration and it is probably the primary cause of many HD symptoms 8,9

This effect was mediated through decline of IgE elevation and stimulation of IFN-

doi: 10.1038/ejcn.2017.132 31

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