Abstract
It is becoming more evident that histone acetylation, as one of the epigenetic modifications or markers, plays a key role in the etiology of Alzheimer’s disease (AD). Histone acetylases and histone deacetylases (HDACs) are the well-known covalent enzymes that modify the reversible acetylation of lysine residues in histone amino-terminal domains. In AD, however, the roles of these enzymes are controversial. Some recent studies indicate that HDAC inhibitors are neuroprotective by regulating memory and synaptic dysfunctions in cellular and animal models of AD; while on the other hand, increase of histone acetylation have been implicated in AD pathology. In this review, we focus on the recent advances on the roles of histone acetylation covalent enzymes in AD and discuss how targeting these enzymes can ultimately lead to therapeutic approaches for treating AD.
Highlights
Introduction toAlzheimer’s DiseaseAlzheimer’s disease (AD) is well known for the symptom of progressive memory loss
We focus on the recent advances on the roles of histone acetylation covalent enzymes in AD and discuss how targeting these enzymes can lead to therapeutic approaches for treating AD
We found that H3 in the promoters of presenilin 1 (PS1) and BACE1, a β-secretase to amyloid precursor protein (APP) for Aβ peptides, is hyperacetylated in N2a cells transfected with Swedish mutated APP (Lu et al, 2014)
Summary
The molecular and clinical implications of the HDAC inhibitors were initially identified in cancer therapy (Carew et al, 2008). Khan et al compared the clinically relevant HDAC inhibitors against the rhHDAC (recombinant human HDAC) microforms and identified the potency and selectivity of ten microforms that increase histone acetylation in Hela cells (Khan et al, 2008). The HDAC inhibitors are likely to modulate transcriptional programs of certain relatively specific genes (Fischer et al, 2007)
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