Histone deacetylase inhibitors preserve function in aging axons

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

Abstract

Aging increases the vulnerability of aging white matter to ischemic injury. Histone deacetylase (HDAC) inhibitors preserve young adult white matter structure and function during ischemia by conserving ATP and reducing excitotoxicity. In isolated optic nerve from 12-month-old mice, deprived of oxygen and glucose, we show that pan- and Class I-specific HDAC inhibitors promote functional recovery of axons. This protection correlates with preservation of axonal mitochondria. The cellular expression of HDAC 3 in the central nervous system (CNS), and HDAC 2 in optic nerve considerably changed with age, expanding to more cytoplasmic domains from nuclear compartments, suggesting that changes in glial cell protein acetylation may confer protection to aging axons. Our results indicate that manipulation of HDAC activities in glial cells may have a universal potential for stroke therapy across age groups.

Original languageEnglish (US)
Pages (from-to)108-115
Number of pages8
JournalJournal of neurochemistry
Volume123
Issue numberSUPPL. 2
DOIs
StatePublished - Nov 2012
Externally publishedYes

Keywords

  • aging
  • histone deacetylase
  • ischemia
  • mouse optic nerve
  • neuroprotection

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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