Current Biol：亨廷顿病患者的基因突变可促进其学习能力提高

“携带有遗传突变的亨廷顿病症患者比正常人群学习地更快，而且其遗传突变越显著，其学习能力越强，”刊登在国际杂志<em>Current Biology</em>上的一篇研究报告中，来自波鸿大学的研究者得出了这样的结论。研究小组同时也首次阐述了神经变性疾病和学习能力的增加直接相关。<!--more-->

<br/><strong>通过重复刺激表现出的被动学习</strong><br/>


以前研究中，研究者报道了，通过短期持续重复接受视觉刺激物或可长期改变人们的视觉，参与者的这项任务就是检测刺激所引发的视觉光亮上的改变。当前研究中，相同的研究在29位遗传突变的亨廷顿病（Huntington's disease）患者中进行，这些患者并未表现出任何症状。同时研究者也检测了45个对照人群（无任何基因组突变）。两组参与者中，接受被动刺激物的患者相比没有接受的人群表现出更为有效的学习能力。对于亨廷顿突变患者来说，相比没有突变的参与者来说，其增加了两倍以上的学习能力。

<br/><strong>谷氨酸盐或许具有奇特效应</strong><br/>


神经系统的神经变性疾病基于复杂的改变，其中一种关键的机制就是神经递质-谷氨酸盐释放量的增加。然而谷氨酸盐也是学习能力所必须的，在某些情况下其可以产生奇特的效果：尽管神经细胞处于退化阶段，但是个体的学历能力表现地更好。

<br/><strong>在疾病恶化的情况下检测光亮的差异</strong><br/>


每一个实验组中，电脑上都会有两个连续的小型柱状图，其存在相同或者不同的光亮程度。接受视觉刺激物被动培训之后，分心的刺激物变得并不再有效，刺激物在非相关到相关的特性中涉及的注意力的转移在大脑的脑电图中可以明显呈现出来。

<br/><strong>更强的突变或引发患者更强的表现能力</strong><br/>


在亨廷顿病中，一些短的基因序列是重复的，当疾病爆发的时候，这种重复的次数起着决定性作者。大量重复序列的出现和高学习能力直接相关。这项研究揭示了神经变性的改变可以促使完全相反的效应，这完全颠覆了教条形式所持有的观点。

编译自：<a title="" href="http://www.sciencedaily.com/releases/2012/09/120914080640.htm" target="_blank">Huntington’s Gene Mutation Carriers Learn Faster</a>
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<img src="http://www.bioon.com/biology/UploadFiles/201209/2012091600113296.jpg" alt="" width="113" height="149" border="0" />

<a title="" href="http://dx.doi.org/doi:10.1016/j.cub.2012.08.012" target="_blank">doi:10.1016/j.cub.2012.08.012</a>
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<br/><strong>Faster Perceptual Learning through Excitotoxic Neurodegeneration</strong><br/>


Christian Beste, Edmund Wascher, Hubert R. Dinse, Carsten Saft

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Glutamatergic neural transmission is involved in both neural plasticity [1,2,3] and neurodegeneration [4,5,6]. This combination of roles could result in ambivalent effects in which excitotoxic neurodegeneration augments neural plasticity in parallel. Neural plasticity can be induced by exposure-based learning (EBL) that resembles timing properties of long-term potentiation (LTP) protocols (i.e., LTP-like learning) [7,8]. Even though it has not been demonstrated so far in animal models that perceptual effects of such stimulation protocols are mediated by typical LTP mechanisms, it has been shown that exposure-based learning exerts strong effects on cognitive brain functioning [9] and is modulated by glutamatergic neural transmission [1]. We reveal that exposure-based perceptual learning is more efficient in a human model of excitotoxic neurodegeneration than in healthy participants. Premanifest Huntington's disease gene mutation carriers showed faster increases in perceptual sensitivities than controls. This in turn changed attentional processing in extrastriate visual areas objectified using electroencephalogram data. The emergence of faster learning correlated positively with genetic disease load. Our results confirm an ambivalent action of increased glutamatergic transmission, implying that the process of excitotoxic neurodegeneration is associated with enhanced perceptual learning, which can be used to improve attentional and behavioral control via the alteration of perceptual sensitivities.

<br/>来源：生物谷

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