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Article

Prolonged treatment with pimelic o-aminobenzamide HDAC inhibitors ameliorates the disease phenotype of a Friedreich ataxia mouse model.

Neurobiology of disease - 1 Jun 2011

Sandi Chiranjeevi, Pinto Ricardo Mouro, Al-Mahdawi Sahar, Ezzatizadeh Vahid, Barnes Glenn, Jones Steve, Rusche James R, Gottesfeld Joel M, Pook Mark A

Abstract excerpt

Friedreich ataxia (FRDA) is an inherited neurodegenerative disorder caused by GAA repeat expansion within the FXN gene, leading to epigenetic changes and heterochromatin-mediated gene silencing that result in a frataxin protein deficit. Histone deacetylase (HDAC) inhibitors, including pimelic o-a...

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Identifiers

PMID: 21397024
DOI: 10.1016/j.nbd.2011.02.016
PMCID: PMC3107941

Genes

FXN
GAA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-21397024-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

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Prolonged treatment with pimelic o-aminobenzamide HDAC inhibitors ameliorates the disease phenotype of a Friedreich ataxia mouse model.PMID 21397024Read ↗

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Increasing frataxin gene expression with histone deacetylase inhibitors as a therapeutic approach for Friedreich's ataxiaSemantic proximity Read ↗

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Epigenetic therapy for <scp>F</scp> riedreich ataxiaSemantic proximity Read ↗

HDAC Inhibitors Correct Frataxin Deficiency in a Friedreich Ataxia Mouse ModelSemantic proximity Read ↗

The Friedreich ataxia GAA repeat expansion mutation induces comparable epigenetic changes in human and transgenic mouse brain and heart tissues.Semantic proximity Read ↗

A new FRDA mouse model [Fxnnull:YG8s(GAA) > 800] with more than 800 GAA repeatsSemantic proximity Read ↗

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