Therapeutic application of histone deacetylase inhibitors for central nervous system disorders

sea-maid submitted, created time 2 months 2 weeks (www.nature.com)

Histone deacetylases (HDACs) — enzymes that affect the acetylation status of histones and other important cellular proteins — have been recognized as potentially useful therapeutic targets for a broad range of human disorders. Pharmacological manipulations using small-molecule HDAC inhibitors — which may restore transcriptional balance to neurons, modulate cytoskeletal function, affect immune responses and enhance protein degradation pathways — have been beneficial in various experimental models of brain diseases

Submit comment | Blog It | Email It | Keywords: multiple sclerosis MS Freidreich's ataxia Huntington's disease Rett syndrome histones central nervous system CNS central nervous system disorders histone deacetylase inhibitors

Therapeutic application of histone deacetylase inhibitors for central nervous system disorder

jerry submitted, created time 2 months 2 weeks (www.nature.com)

Histone deacetylases (HDACs) — enzymes that affect the acetylation status of histones and other important cellular proteins — have been recognized as potentially useful therapeutic targets for a broad range of human disorders. Pharmacological manipulations using small-molecule HDAC inhibitors — which may restore transcriptional balance to neurons, modulate cytoskeletal function, affect immune responses and enhance protein degradation pathways — have been beneficial in various experimental models of brain diseases

1 comment | Blog It | Email It | Keywords: multiple sclerosis MS Rubinstein-Taybi syndrome Freidreich's ataxia Rett syndrome Huntington's Huntington's disease central nervous system CNS histones HDAC histone deacetylase

Rett Symptoms Reversed in Mice

technology submitted, created time 1 year 10 months (www.sciencemag.org)

Rett syndrome is an autism spectrum disorder caused by mosaic expression of mutant copies of the X-linked MECP2 gene in neurons. Using a mouse model, the team demonstrated robust phenotypic reversal, as activation of MeCP2 expression leads to striking loss of advanced neurological symptoms in both immature and mature adult animals.

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