Histone acetylation: molecular mnemonics on the chromatin

被引：514

作者：

Graeff, Johannes ^{[1
,2
,3
,4
]}

Tsai, Li-Huei ^{[1
,2
,3
,4
]}

机构：

[1] MIT, Dept Brain & Cognit Sci, Picower Inst Learning & Memory, Cambridge, MA 02139 USA

[2] Harvard Univ, Broad Inst, Cambridge, MA 02142 USA

[3] MIT, Cambridge, MA 02142 USA

[4] MIT, Howard Hughes Med Inst, Cambridge, MA 02139 USA

来源：

NATURE REVIEWS NEUROSCIENCE | 2013年 / 14卷 / 02期

基金：

美国国家卫生研究院;

关键词：

LONG-TERM-MEMORY; TRANSGENIC MOUSE MODEL; RUBINSTEIN-TAYBI-SYNDROME; ALZHEIMERS-DISEASE; SYNAPTIC PLASTICITY; DEACETYLASE INHIBITOR; EPIGENETIC REGULATION; HUNTINGTONS-DISEASE; SODIUM-BUTYRATE; AMYLOID-BETA;

D O I：

10.1038/nrn3427

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Long-lasting memories require specific gene expression programmes that are, in part, orchestrated by epigenetic mechanisms. Of the epigenetic modifications identified in cognitive processes, histone acetylation has spurred considerable interest. Whereas increments in histone acetylation have consistently been shown to favour learning and memory, a lack thereof has been causally implicated in cognitive impairments in neurodevelopmental disorders, neurodegeneration and ageing. As histone acetylation and cognitive functions can be pharmacologically restored by histone deacetylase inhibitors, this epigenetic modification might constitute a molecular memory aid on the chromatin and, by extension, a new template for therapeutic interventions against cognitive frailty.

引用

页码：97 / 111

页数：15

共 180 条

[1]

Chromatin acetylation, memory, and LTP are impaired in CBP+/- mice:: A model for the cognitive deficit in Rubinstein-Taybi syndrome and its amelioration [J].