The Journal of Pathology：老年痴呆症与唇疱疹病毒有关
疱疹病毒（HSV1）很可能是导致阿兹海默症的元凶之一，坊间治疗唇疱疹的便宜药品，或许是用来对付这种最常见痴呆疾病的有效利器。
《泰晤士报》六日独家报导，英国曼彻斯特大学科学家发现，罹患阿兹海默症的病患有多达六○％体内有唇疱疹病毒。尽管这只是初步研究，却可能改变科学界对这种脑部疾病的认识，从而开启治疗阿兹海默症的新途径。目前光是英国，便有超过四十万阿兹海默症患者。
阿兹海默症病患 六成验出病毒
据中国时报引述报道，领导这项研究的露丝．伊兹哈基教授说，令人感到振奋的是，用来对付唇疱疹病毒的药物已问世一段时日，这类药品既便宜，一般人服用也不会有副作用。如果唇疱疹病毒确实会引发阿兹海默症，未来相关研究的进展将会非常快速。
医学界认为，脑细胞中的“贝它糊蛋白”（beta amyloid protein）斑块堆积，是造成阿兹海默症的主要原因，而唇疱疹病毒可能在这种斑块形成时扮演重要角色。
伊兹哈基教授的团队研究贝它糊蛋白斑块的形成已有数年。去年他们发表报告指出，在实验室进行细胞培养时，唇疱疹病毒能助长贝它糊蛋白斑块的形成。
这次他们在《病理学期刊》发表的新研究报告更迈前一大步，内容宣称他们在阿兹海默症患者脑细胞的蛋白斑块中，发现唇疱疹病毒感染的坚定证据。
研究人员利用“原位聚合？连锁反应”（IS-PCR）的精密基因分析技术，在蛋白斑块中侦测到唇疱疹病毒的DNA，显示这种病毒有可能导致蛋白斑块形成。
两者关连与疗效 五年后见真章
伊兹哈基教授希望筹措到资金，展开动物实验，希望能以一年左右的时间确认唇疱疹病毒真的与阿兹海默症有关。接下来，他们将在临床实验中，测试抗病毒药对阿兹海默症初期病患的疗效，这大约需要三到五年时间。
感染唇疱疹病毒的情况相当普遍，大部分成年人感染过这种病毒，其中二○至四○％会长出唇疱疹。上述研究并不意味感染唇疱疹病毒每个人或大多数人会罹患阿兹海默症。就算证实这种病毒与阿兹海默症有关，它也并非唯一成因，其它还包括某些遗传因素。（生物谷Bioon.com）
生物谷推荐原始出处：
The Journal of Pathology, Volume 217, Issue 1 , Pages131 - 138 DOI: 10.1002/path.2449
Herpes simplex virus type 1 DNA is located within Alzheimer's disease amyloid plaques
MA Wozniak 1, AP Mee 2 a, RF Itzhaki 1 *
1Faculty of Life Sciences, University of Manchester, UK
2Department of Medicine, Manchester Royal Infirmary, UK
The brains of Alzheimer's disease sufferers are characterized by amyloid plaques and neurofibrillary tangles. However, the cause(s) of these features and those of the disease are unknown, in sporadic cases. We previously showed that herpes simplex virus type 1 is a strong risk factor for Alzheimer's disease when in the brains of possessors of the type 4 allele of the apolipoprotein E gene (APOE-ε4), and that β-amyloid, the main component of plaques, accumulates in herpes simplex virus type 1-infected cell cultures and mouse brain. The present study aimed to elucidate the relationship of the virus to plaques by determining their proximity in human brain sections. We used in situ polymerase chain reaction to detect herpes simplex virus type 1 DNA, and immunohistochemistry or thioflavin S staining to detect amyloid plaques. We discovered a striking localization of herpes simplex virus type 1 DNA within plaques: in Alzheimer's disease brains, 90% of the plaques contained the viral DNA and 72% of the DNA was associated with plaques; in aged normal brains, which contain amyloid plaques at a lower frequency, 80% of plaques contained herpes simplex virus type 1 DNA but only 24% of the viral DNA was plaque-associated (p < 0.001). We suggest that this is because in aged normal individuals, there is a lesser production and/or greater removal of β-amyloid (Aβ), so that less of the viral DNA is seen to be associated with Aβ in the brain. Our present data, together with our finding of Aβ accumulation in herpes simplex virus type 1-infected cells and mouse brain, suggest that this virus is a major cause of amyloid plaques and hence probably a significant aetiological factor in Alzheimer's disease. They point to the usage of antiviral agents to treat the disease and possibly of vaccination to prevent it. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
