Researchers report that rodents with the mutant huntingtin gene exhibited reduced anxiety, as indicated by reduced vocalization and increased risk taking; reduced generation of neurons and oligodendrocytes from progenitor and stem cells in vitro; and imbalances in brain neurotransmitter signaling, compared with controls carrying the wild-type huntingtin gene; presymptomatic treatment with the histone deacetylase inhibitor LBH589 reversed some of the molecular, cellular, and behavioral changes tied to the mutant gene, suggesting a potential early therapeutic approach for Huntington disease, the symptoms of which typically manifest during adulthood.
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Article #18-07962: "Early postnatal behavioral, cellular, and molecular changes in models of Huntington disease are reversible by HDAC inhibition," by Florian A. Siebzehnrubl et al.
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Proceedings of the National Academy of Sciences