美国开发“大脑伟哥” 人类记忆力将被改变

最近,一种被戏称为“大脑伟哥”的能够提高记忆力的药物，即将在美国通过人体试验，预计可能在五年内投入市场。这种药物通过作用于大脑记忆的形成过程，达到提高记忆力的目的。

　　药物的发明者遗传学教授提姆-塔利说：“如果试验能被证明安全和有效，它最终会被那些想学一门语言或弹奏一种乐器的人使用，甚至将被用于学校。”但最大的市场将来自于那些记忆力正在减退的四五十岁的健康人。

　　这种药物代码为HT-0712，能使短期记忆的信息长期保持。它能够激活人类细胞中的一种基因，这种基因一旦被激活，它将使大脑细胞产生对记忆形成过程来说非常重要的联接。对大多数人来说，记忆形成的能力随着年龄的增长而下降，最终导致健忘。

　　今年夏天，在美国100个带有轻度记忆力损伤的人将接受这种药物试验，以检验药物的安全性和有效性。塔利教授希望这种药物能够帮助这些病人提高记忆力，修复这些早期痴呆者的记忆损伤。如果试验成功，将进行更大规模的试验，争取在五到七年内能够投入生产。塔利教授说，现在就预言这种药物的价值还嫌太早。

　　进行人身试验的决定，是取得了在果蝇身上试验的成功后做出的。注射了这种药物的果蝇在仅仅遭遇一次后，就学会了躲避有害的化学物质。而没有注射这种药物的果蝇在最终学会躲避之前，暴露在有害化学物质中的次数平均是前者的10倍。

　　相似的，把这种药物的口服剂在训练前20分钟或在训练后60分钟给老鼠服下，结果有效地提高了老鼠的记忆力。

　　尽管如此，这种增进记忆疗法不一定绝对安全，它将被滥用。神经生物学教授史蒂文-罗斯说：“我想，它会像运动员使用合成类固醇一样，将变得无法控制。我们将不得不学会和它们一起生活。”

Tim Tully
Professor
Ph.D., University of Illinois, 1981
Genetic basis of memory
email tully@cshl.edu, phone (516) 367-8455, fax (516) 367-8496
To understand the biological basis of memory, a neurogenetic perspective asks, 揥hat genes in the genome, when mutated, can produce learning/memory disabilities??An adequate answer to this question will include the identification of (i) genes involved in molecular mechanisms of cellular plasticity, (ii) genes involved in the development of underlying neural architectures, and (iii) genes involved in neurodevelopment and in the ongoing function of terminally differentiated neurons. Such a comprehensive genetic etiology of memory will lead initially to a valid biological categorization of cognitive dysfunction and finally to more effective behavioral and pharmacological therapies for memory loss.

Obviously, hundreds of genes will likely be involved in a complex emergent function such as memory formation. Few genes, however, currently have been identified. Hence, efforts now must be focused on new gene discovery. Detailed studies of Pavlovian olfactory conditioning in the fruit fly have revealed behavioral properties that are quite similar to those characterized for other tasks in other vertebrate and invertebrate species. Molecular identification of Drosophila genes involved with olfactory learning supports this notion. Disruptions of several enzymatic components of the cAMP second messenger system all produce olfactory learning/memory deficits. In particular, transgenic manipulations of the cAMP-responsive transcription factor, CREB, have produced a 損hotographic?memory in fruit flies.

These observations demonstrate that regulation of gene expression underlies the formation of new long-term memories most likely via the growth of new synapses. This cascade of molecular and cellular events will be elucidated further with continued study of gene function in various animal model systems.

Selected Publications

Yin, J.C.P., M. Del Vecchio, H. Zhou, and T. Tully. 1995. CREB as a memory modulator: Induced expression of a dCREB2 activator isoform enhances long-term memory in Drosophila. Cell 81: 107–115.

Rohrbough, J., S. Pinto, R.M. Mihalek, T. Tully, and K. Broadie. 1999. latheo, a Drosophila gene involved in learning, regulates functional synaptic plasticity. Neuron 23: 55–70.

DeZazzo J., D. Sandstrom, S. de Belle, K. Velinzon, P. Smith, L. Grady, M. Del Vecchio, M. Ramaswami, and T. Tully. 2000. nalyot, a mutation of the Drosophila Myb-related Adf1 transcription factor, disrupts synapse formation and olfactory memory. Neuron 27: 145–158.

Dubnau, J., L. Grady, T. Kitamoto, and T. Tully. 2001. Disruption of neurotransmission in Drosophila mushroom body blocks retrieval but not acquisition of memory. Nature 411: 476–480.

Tully, T. 2003. Pavlov’s Dogs. Curr. Biol. 13: R117–R119.
http://www.cshl.org/public/SCIENCE/tully.html

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美国开发“大脑伟哥” 人类记忆力将被改变