Author: Holly B Kordasiewicz

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Preprints

Alpha-synuclein antisense oligonucleotides as a disease-modifying therapy for Parkinson's disease

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Huntingtin lowering reduces somatic instability at CAG-expanded loci

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Altered Huntingtin-Chromatin Interactions Predict Transcriptional and Epigenetic Changes in Huntingtons Disease

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Prion protein lowering is a disease-modifying therapy across prion strains, disease stages, and endpoints

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An antisense oligonucleotide leads to suppressed transcriptional elongation of Hdac2 and long-term memory enhancement

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  • In pharmacology and toxicology: 288
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Peripheral Htt silencing does not ameliorate central signs of disease in the B6.HttQ111/+ mouse model of Huntington's Disease

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  • In neuroscience: 7,685
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Characterization of the prion protein binding properties of antisense oligonucleotides

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  • In biochemistry: 3,093
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Regional variability, genotypic effects, and pharmacodynamic impact on prion protein concentration in the central nervous system

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