The Rubinstein-Taybi syndrome: modeling mental impairment in the mouse

被引:24
作者
Barco, A. [1 ]
机构
[1] CSIC, UMH, Inst Neurociencias Alicante, Sant Joan dAlacant, Spain
关键词
CREB-binding protein; mental impairment; mouse model; Rubinstein-Taybi syndrome; CREB-BINDING-PROTEIN; HISTONE ACETYLTRANSFERASE ACTIVITY; TRANSCRIPTIONAL COACTIVATOR CBP; LONG-TERM-MEMORY; SYNAPTIC PLASTICITY; HUNTINGTONS-DISEASE; TRUNCATED FORM; DNA-BINDING; IN-VITRO; KAPPA-B;
D O I
10.1111/j.1601-183X.2007.00320.x
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
Mental impairment syndromes are diagnosed based on below-average general intellectual function originated during developmental periods. Intellectual abilities rely on the capability of our brain to obtain, process, store and retrieve information. Advances in the past decade on the molecular basis of memory have led to a better understanding of how a normal brain works but also have shed new light on our understanding of many pathologies of the nervous system, including diverse syndromes involving mental impairment. The recent multidisciplinary analysis of various mouse models for Rubinstein-Taybi syndrome has shown the power of animal models to produce an important leap forward in our understanding of a complex mental disease while simultaneously opening new avenues for its treatment. These studies also suggest that some of the cognitive and physiological deficits observed in mental impairment syndromes may not simply be caused by defects originated during development but may result from the continued requirement of specific enzymatic activities throughout life.
引用
收藏
页码:32 / 39
页数:8
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