google一下，这篇12月14日在线发表，免费下载的文章已经被全世界的医学新闻大量报道：

 

因为作者选择的是BDNF的神经营养因子途径，而不是一直以来AD学界最关注的Aβ的生成与降解途径，全文摘要如下：

 

Currently, the major drug discovery paradigm for neurodegenerative diseases is based upon high affinity ligands for single disease-specific targets. For Alzheimer’s disease (AD), the focus is the amyloid beta peptide (Aß) that mediates familial Alzheimer’s disease pathology. However, given that age is the greatest risk factor for AD, we explored an alternative drug discovery scheme that is based upon efficacy in multiple cell culture models of age-associated pathologies rather than exclusively amyloid metabolism. Using this approach, we identified an exceptionally potent, orally active, neurotrophic molecule that facilitates memory in normal rodents, and prevents the loss of synaptic proteins and cognitive decline in a transgenic AD mouse model.

 

无疑，此方向将再次强化对衰老与神经营养衰减的关系认识的刷新。

 

 

补充说明，第一作者： Qi Chen， a former Salk postdoctoral researcher, working in Salk's Cellular Neurobiology Laboratory headed by David Schubert