Cell-Intrinsic Glial Pathology Is Conserved across Human and Murine Models of Huntington’s Disease

The authors investigated mutant HTT-associated changes in gene expression by mouse and human striatal astrocytes, as well as in mouse microglia, to identify commonalities in glial pathobiology across species and models.
[Cell Reports]
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UVB Protective Effects of Sargassum horneri through the Regulation of Nrf2 Mediated Antioxidant Mechanism

Scientists aimed to evaluate the protective effect of a methanol extract of Sargassum horneri (SHM), which contains 6-hydroxy-4,4,7a-trimethyl-5,6,7,7a-tetrahydrobenzofuran-2(4H)-one (HTT) and apo-9′-fucoxanthinone, against ultraviolet B (UVB)-induced cellular damage in human keratinocytes and its underlying mechanism.
[Scientific Reports]
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Impaired Inhibitory GABAergic Synaptic Transmission and Transcription Studied in Single Neurons by Patch-Seq in Huntington’s Disease

Investigators found that expression of mutant Htt decreased the synaptic output of striatal neurons in a cell autonomous fashion and identified a number of genes whose dysregulation was correlated with physiological deficiencies in mutant Htt neurons.
[Proceedings of the National Academy of Sciences of the United States of America]
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Impaired Inhibitory GABAergic Synaptic Transmission and Transcription Studied in Single Neurons by Patch-Seq in Huntington’s Disease

we demonstrated that Patch-seq technology can be applied both to better understand molecular mechanisms underlying a complex neurological disease at the single-cell level and to provide a platform for screening for therapeutics for the disease.
[Proceedings of the National Academy of Sciences of the United States of America]
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PIAS1 Modulates Striatal Transcription, DNA Damage Repair, and SUMOylation with Relevance to Huntington’s Disease

Investigators evaluated the mechanistic contributions of protein inhibitor of activated STAT-1 (PIAS1) in Huntington’s disease (HD) mice and HD patient-derived induced pluripotent stem cells and found a link between PIAS1 and DNA damage repair pathways.
[Proceedings of the National Academy of Sciences of the United States of America]
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