Neurotransmitters and Drugs, Second Ed
Neurotransmitters and Drugs, Second Ed
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神经递质和药物，第二版
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发表时间：
1984
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通讯作者：
Eamonn Kelly
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作者：
Eamonn Kelly
自从在新几内亚发现库鲁病并将其传播给黑猩猩以来，对人类中枢神经系统慢性和亚急性退行性疾病的研究迅速增加。目前正在特别关注进行性多灶性白质脑病（pml）及其与乳头样病毒的可能关系；亚急性硬化性全脑炎及其与麻疹的关系；蜱传俄罗斯春夏脑病复合体毒株引起的部分连续性癫痫和其他慢性局灶性神经综合征；先天性风疹与脑巨细胞病毒；3例亚急性脑炎伴单纯疱疹；与32型腺病毒相关的脑炎；4 .海绵状克雅型老年痴呆；和库鲁病。再加上动物身上的疾病，如痒病、水貂脑病和visnamaedi复体，很明显，有很多宿主可能患有潜在的传染性慢性退行性中枢神经系统疾病。visna-maedi复体很重要，因为这种病毒既可以引起慢性肺部疾病，也可以引起中枢神经系统疾病在这两种情况下都有细胞增殖；在中枢神经系统中，神经胶质细胞的某些细胞受到影响，在肺中，病变发生在细支气管上皮。最近一期的《临床研究年鉴》报道了在这些“慢病毒疾病”方面的一些重要新发现，其中包括对多发性硬化症如何在同样的背景下加以考虑的评论。海绵状脑病——库鲁病、c.j.、痒病和水貂脑病引起了特别的兴趣。其中一个原因是代理人的特殊性质；7 .耐热失活、蛋白水解酶、乙基乙胺、甲醛、RNase、DNase，以及对紫外光失活的极强抵抗力。这导致人们猜测，它们是缺乏核酸的病原体，能够以一种不寻常的方式复制。膜破坏物质会引起痒病的失活，提示可能与复制膜或膜相关多糖有关。最近，人们对痒病病原体与非常小的RNA马铃薯纺锤体病毒和菊花树桩病毒进行了有趣的比较，这些病毒有时被称为类病毒，因为它们比任何已知的病毒都小得多为了使这一假设得到证实，痒病病原体必须被证明具有核酸。到目前为止，这似乎不太可能，但核酸牢牢地结合在膜上仍然可能被发现，最近在痒病的大脑中发现了微量的小单链DNA
Since the discovery ofKuru in New Guinea' and its transmission to the chimpanzee,2 research into chronic and subacute degenerative diseases ofthe human central nervous system has rapidly increased. Particular attention is being given to progressive multifocal leukoencephalopathy (P.M.L.) and its possible relationship to a papova-like virus; subacute sclerosing panencephalitis (S.S.P.E.) and its relationship to measles; epilepsia partialis continua and other chronic focal neurological syndromes caused by strains of the tick-borne Russian spring summer (R.S.S.) encephalitic complex; congenital rubella and cytomegalovirus in the brain;3 subacute encephalitis with herpes simplex; encephalitis associated with adenovirus type 32;4 presenile dementia of the spongiform CreuzfeldtJakob (C.J.) type; and Kuru. Add to these the diseases in animals such as scrapie, mink encephalopathy, and the visnamaedi complex, and it is evident that there is a wide range of hosts which may suffer potentially transmissible chronic degenerative diseases of the C.N.S. The visna-maedi complex is important because the virus can cause both chronic lung and C.N.S. disease.5 In both conditions there is cell proliferation; in the C.N.S. certain cells of the glia are affected and in the lungs lesions occur in the epithelium of the bronchioles. A recent edition of the Annals of Clinical Research6 reports on some of the important new findings in these "slow virus diseases," and it includes comment on how multiple sclerosis may have to be considered in the same context. The group of diseases called the spongiform encephalopathies-Kuru, C. J., scrapie, and mink encephalopathy arouse particular interest. One reason for this is the extraordinary nature of the agents ;7 their resistance to heat inactivation, proteolytic enzymes, acetylethyleneamine, formaldehyde, RNase, DNase, and their extreme resistance to ultraviolet light inactivation. This has led to speculation that they are agents which lack nucleic acid and are able to replicate in an unusual way. Membrane disrupting substances will cause inactivation in scrapie, suggesting that a replicating membrane or a membrane associated polysaccharide may be concerned. An interesting comparison has been made recently between the scrapie agent and the very small size RNA potato-spindletuber-virus and chrysanthemum-stump-virus, sometimes termed viroids because they are much smaller than any known viruses.8 For this hypothesis to be substantiated the scrapie agent will have to be shown to possess nucleic acid. To date this seems unlikely, but nucleic acid firmly bound to membrane may still be found, and the recent finding oftrace amounts of a small, single stranded DNA in scrapie brain and its apparent