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
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Reduction in SCFAs synthesis due to intestinal dysbiosis encourages pancreatic - cell proliferation, insulin production, and glucose tolerance, showing that these impacts are dependent on short-chain fatty acid receptors FFA2 and FFA3 in mouse model system (253)