虽然大多数阿尔茨海默氏症的治疗研究集中在beta淀粉样多肽上，一个新的方法显示，在小鼠模型中将tau蛋白质的内部生产减少50%，能防止该病认知方面的问题。阿尔茨海默氏症是最常见的痴呆症，患者的大脑中有与tau蛋白质沉淀物纠缠在一起的神经元，也有淀粉样多肽的斑块，但是人们不清楚这两种东西对作为疾病特征的智力障碍如何起作用。Erik D. Roberson和同事还显示tau在神经元健康上起关键作用，这就是为什么减少其产生也许能对阿尔茨海默氏症和其他神经紊乱症起保护作用的原因。这些研究人员在小鼠模型中没有发现减少tau的副作用。
原始出处:
Science 4 May 2007:
Vol. 316. no. 5825, pp. 750 - 754
DOI: 10.1126/science.1141736
Reports
Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model
Erik D. Roberson,1,2* Kimberly Scearce-Levie,1,2 Jorge J. Palop,1,2 Fengrong Yan,1 Irene H. Cheng,1,2 Tiffany Wu,1 Hilary Gerstein,1 Gui-Qiu Yu,1 Lennart Mucke1,2*
Many potential treatments for Alzheimer's disease target amyloid-ß peptides (Aß), which are widely presumed to cause the disease. The microtubule-associated protein tau is also involved in the disease, but it is unclear whether treatments aimed at tau could block Aß-induced cognitive impairments. Here, we found that reducing endogenous tau levels prevented behavioral deficits in transgenic mice expressing human amyloid precursor protein, without altering their high Aß levels. Tau reduction also protected both transgenic and nontransgenic mice against excitotoxicity. Thus, tau reduction can block Aß- and excitotoxin-induced neuronal dysfunction and may represent an effective strategy for treating Alzheimer's disease and related conditions.
1 Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA.
2 Department of Neurology, University of California, San Francisco, CA 94158, USA.
* To whom correspondence should be addressed. E-mail: eroberson@gladstone.ucsf.edu (E.D.R.); lmucke@gladstone.ucsf.edu (L.M.)
