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Kai Shing

As seen in: BioRxiv
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Articles by Kai Shing

Early whole-body mutant huntingtin lowering averts changes in proteins and lipids important for synapse function and white matter maintenance in the LacQ140 mouse model

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By Kai Shing, Ellen Sapp, Adel Boudi, Sophia Liu
| BioRxiv
Abstract Expansion of a triplet repeat tract in exon1 of the HTT gene causes Huntington's disease (HD). The mutant HTT protein (mHTT) has numerous aberrant interactions with diverse, pleiomorphic effects. No disease modifying treatments exist but lowering mutant huntingtin (mHTT) by gene therapy is a promising approach to treat Huntington's disease (HD). It is not clear when lowering should be initiated, how much lowering is necessary and for what duration lowering should occur to achieve benefits.
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Early whole-body mutant huntingtin lowering preserves proteins and lipids important for synapse function and white matter maintenance in the LacQ140 mouse model

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By Ellen Sapp, Kai Shing, Adel Boudi, Sophia Liu
| BioRxiv
Abstract Lowering mutant huntingtin (mHTT) transcription is a promising approach to treat Huntington's disease (HD). Using a mHtt-inducible mouse model we analyzed mHtt lowering initiated at different ages and sustained for different time-periods. mHTT protein in cytoplasmic and synaptic compartments of the caudate putamen, which is most affected in HD, was reduced 38-52%. Little or no lowering of mHTT occurred in nuclear and perinuclear regions where aggregates formed at 12 months of age.
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