Epigenetic histone acetylation and deacetylation mechanisms in experimental models of neurodegenerative disorders.

Abstract:

INTRODUCTION:Epigenetic modifications, such as histone acetylation and deacetylation, are responsible for maintaining chromatin stability. As such, they have been implicated in a wide range of neurodegenerative disorders. METHODS:Histone acetylation involves the presentation of an acetyl group to lysine residues at the N terminus of histone proteins. Conversely, histone deacetylation involves the detachment of acetyl groups. Transcriptionally active chromatin is linked to acetylated histones, and in mouse neurons, is implicated in proper learning and memory. DISCUSSION:Proper functioning of histone deacetylases (HDACs) plays a pivotal role in histone acetylation homeostasis. RESULTS:A wide range of brain disorders are associated with improper balances within histone acetylation mechanisms, resulting in transcriptional dysfunction and translational disparities. Treatment modalities with various HDAC inhibitors have emerged as potential new strategies for therapeutic intervention in neurodegenerative disease. HDAC inhibitors enhance synaptic plasticity, learning and memory in neurodegenerative disorders, such as Alzheimer's disease (AD), Huntington's disease (HD) and Parkinson's disease (PD). In this review, we discuss a variety of in vitro cellular models and in vivo mouse models of neurodegenerative diseases and the potential application of HDAC inhibitors to prevent and treat these disorders.

authors

Konsoula Z,Barile FA

doi

10.1016/j.vascn.2012.08.001

subject

Has Abstract

pub_date

2012-11-01 00:00:00

pages

215-20

issue

3

eissn

1056-8719

issn

1873-488X

pii

S1056-8719(12)00088-3

journal_volume

66

pub_type

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