生物谷报道：是否能够有一种药物来促进记忆、甚至还能恢复在阿尔茨海默氏症等疾病中遗忘的记忆？发表在5月10日的《自然》杂志上的一篇报道用一种严重神经退行性疾病动物模型（CK-p25 Tg小鼠）所做的新的研究工作让我们看到了这种希望。
在这项研究中，研究人员用两种办法恢复了这些实验鼠的学习和长期记忆——一种是进行环境强化（基本上就是使生活变得有趣）；另一种是用“组蛋白去乙酰基转移酶”（HDAC）抑制剂来处理。HDAC被认为能够通过促进组蛋白乙酰化作用、从而改变细胞核中的转录来帮助正常个体记忆的形成。值得注意的是，这种记忆促进作用在严重脑萎缩的p25实验鼠身上也出现了。记忆的恢复与已有神经网络的重新排列有关，这可能是恢复长期记忆的一个手段。
FIGURE 1. Environmental enrichment reinstates learning in CK-p25 Tg mice after neurodegeneration.
a, Experimental design (n = 8 per group). The experiment starts with the induction of p25 in CK-p25 Tg mice (0 weeks). b, Enriched and non-enriched CK-p25 Tg mice displayed similar brain atrophy (***P < 0.0001 versus control). c, Non-enriched CK-p25 Tg mice displayed impaired associative learning (P = 0.0337 versus control), whereas enriched CK-p25 Tg mice were improved when compared to the non-enriched group (***P < 0.0001). d, Enriched CK-p25 Tg mice performed significantly better in the water maze test than non-enriched CK-p25 mice (F1, 568 = 77.167; ***P < 0.0001 versus control), but were still inferior to the no-p25 group (F1, 568 = 49.453; P < 0.0001). e, Hippocampal lysates were analysed for neuronal and synaptic protein levels (*P < 0.05 enriched versus non enriched CK-p25 Tg, n = 3). f, Enriched CK-p25 Tg mice displayed significantly increased hippocampal synaptophysin immunoreactivity when compared to non-enriched CK-p25 Tg mice (*P = 0.0304). Scale bar, 20 m. py, pyramidal cell layer; SVP, synaptophysin. Error bars indicate s.e.m.
原文出处：
Nature Volume 447 Number 7141
Recovery of learning and memory is associated with chromatin remodelling p178
Andre Fischer, Farahnaz Sananbenesi, Xinyu Wang, Matthew Dobbin & Li-Huei Tsai
doi:10.1038/nature05772
Abstract | Full Text | PDF (1,569K) | Supplementary information
See also: Editor's summary | News and Views by Sweatt
作者简介：
Li-Huei Tsai, Ph.D.
Dr. Tsai is also Picower Professor of Neuroscience in the Department of Brain and Cognitive Sciences at the Massachusetts Institute of Technology. She received her Ph.D. degree from the University of Texas Southwestern Medical Center at Dallas under the direction of Bradford Ozanne. She then joined Ed Harlow's laboratory at Cold Spring Harbor Laboratory and Massachusetts General Hospital for postdoctoral training. Prior to her move to MIT, Dr. Tsai was Professor of Pathology at Harvard Medical School.
RESEARCH ABSTRACT SUMMARY:
Li-Huei Tsai is interested in the mechanisms that underlie the production and positioning of neurons during brain development, signaling at synapses, and the demise of the nervous system in adult life.
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